Common complications induced by diabetes.😰😰😰

Diabetes is a chronic metabolic disease. Diabetes can easily lead to other disorders. Most patients with diabetes generally have other unhealthy conditions or diseases, not just diabetes. Diabetes can also exacerbate these unhealthy conditions or diseases. Complications that diabetes can easily induce are pointed out below.

1. Eye disease.

Diabetes is a risk factor for many eye diseases.

Cataracts: Cataracts are closely related to age. It is one of the leading causes of blindness in the elderly. Apart from age-related, diabetes is also a risk factor for cataracts.

Glaucoma: People with diabetes are more likely to have glaucoma than people without diabetes.

Dry Eye: It is a very common eye disease. People with diabetes are also more likely to suffer from dry eye syndrome. Diabetes is a significant risk factor for dry eye disease.

2. Oral disease.

People with diabetes are more likely to have oral disease than people without diabetes. And they have a significantly increase in disease severity and duration. Diabetes is a risk factor for periodontitis. Periodontitis is also a common complication of diabetes. The risk of periodontitis in people with diabetes is nearly three times greater than in people without diabetes.

3. Kidney disease.

One of the main causes of chronic kidney disease is kidney disease caused by diabetes. Although the research on the pathogenesis and etiology of diabetic nephropathy is not complete, it is generally believed that it is caused by many risk factors, such as age, blood pressure, obesity, genetic susceptibility, glycemic control, glomerular filtration rate. 

4. Neuropathy.

Another common chronic complication of diabetes is diabetic neuropathy. Both the central and peripheral nerves may be affected. It is a heterogeneous group of diseases with a variety of different clinical manifestations. The most common diabetic peripheral neuropathy is distal symmetrical polyneuropathy. About 75% of diabetic neuropathy is this neuropathy, and it is one of the major risk factors for diabetic foot ulcers. It is also the leading cause of falls and fractures in people with diabetes.

5. Fractures.

People with diabetes have a significantly higher fracture risk than people without diabetes. Fractures in people with diabetes are not due to calcium or vitamin D deficiency. Some studies have pointed out that in the case of long-term hyperglycemia, changes in collagen cross-linking and glycosylation products can cause changes in the microstructure of bones. It causes bone to become brittle and more prone to fractures.

6. Mental illness.

Although mental illness is not a particularly common complication of diabetes, it can also occur due to the effects of diabetes on the central nervous system and cerebrovascular. Especially in older people with diabetes, they are prone to symptoms of memory loss and diabetes may exacerbate this condition. In addition, depression is the most common symptom of mental illness.

7. Cancer.

There are many studies showing that the risk of various cancers such as gastrointestinal cancer, liver cancer, pancreatic cancer, ovarian cancer, etc. is increased in diabetic patients. Among them, the risk of pancreatic cancer, colorectal cancer, bladder cancer, endometrial cancer and breast cancer is more than twice that of the general population. In addition, studies have shown that for every 1% increase in HbA1c in diabetic patients, the risk of cancer will increase by 18%.

8. Cardiovascular and cerebrovascular disease.

People with diabetes are more likely to have atherosclerosis and it progresses more rapidly than the normal population. It can in turn cause other cardiovascular diseases such as coronary heart disease. Studies have shown that patients with type 1 diabetes significantly increase the prevalence of myocardial infarction, heart failure, coronary heart disease, and atrial fibrillation. Increasing age and duration of diabetes also increases the prevalence of lower extremity atherosclerotic disease. It increases the risk of death from cardiovascular disease in people with diabetes. Cardiac autonomic neuropathy may also occur in people with diabetes. The risk of stroke increases by 1.5 to 4 times with type 2 diabetes. One of the risk factors for stroke is diabetes. The risk of cerebrovascular disease such as ischemic stroke is highly correlated with type 2 diabetes and high levels of HbA1c.

9. Infection.

The risk of many infections, such as head and neck infections, respiratory infections, skin and soft tissue infections, gastrointestinal infections, blood infections, etc., is significantly increased with diabetes. Blood vessels and neuropathy in the distal lower extremities can lead to diabetic foot infections and ulcers in the feet of people with diabetes. Severe cases can lead to amputation and death.

10. Hepatobiliary disease.

Because people with diabetes have a higher area of visceral adipose tissue than normal people, they are more likely to develop hepatic steatosis, which can lead to liver disease. People with diabetes are also more likely to have gallstones.

11. Blood disease.

Adults with diabetes have a higher risk of anemia. It is related to the patient's gender, disease course and comorbidities. Women have a higher risk of anemia than men. Patients with longer disease duration and comorbidities are also more likely to develop anemia.

12. Others.

Diabetes increases or worsens the risk of many diseases such as thyroid disease, dementia, and electrolyte disturbances. Clinical treatment should also pay attention to these problems.

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Introduction of α-glucosidase inhibitors.📋📋📋

Diabetes is a very common chronic disease. With the development of social economy, the incidence of diabetes is getting higher and higher, and it has a younger trend. There are many types of hypoglycemic drugs. One of the common clinical hypoglycemic drugs is α-glucosidase inhibitors. How does an α-glucosidase inhibitor work and what is the difference between different α-glucosidase inhibitors?

Common α-glucosidase inhibitors.

Acarbose, voglibose and miglitol are common alpha-glucosidase inhibitors. 

• Acarbose is obtained by the direct extraction and isolation of secondary metabolites of Actinomycetes.
• Voglibose is obtained by modifying the structure of secondary metabolites of Actinomycetes.
• Miglitol is obtained by structural modification of secondary metabolites of Bacillus.

Acarbose

Voglibose

Miglitol

Mechanism of action of α-glucosidase inhibitors.

Monosaccharides (such as glucose, fructose, and galactose), disaccharides (such as sucrose, maltose), and polysaccharides (such as starch) are sugars in food. They are the most important energy substances in the human body. Small intestinal epithelial cells can directly absorb monosaccharides. Disaccharides and polysaccharides require α-glucosidase to hydrolyze them into monosaccharides for reabsorption. Therefore, when α-glucosidase activity is inhibited, the absorption of sugar can be reduced. α-glucosidase is a general term for carbohydrases such as sucrase, lactase, maltase, isomaltase, and alpha-critical dextrinase. α-glucosidase inhibitors are structurally similar to disaccharides or polysaccharides. It binds to α-glucosidase and inhibits its activity. It reduces the breakdown of these sugars into simple sugars, thereby reducing sugar absorption. It can effectively reduce glycosylated hemoglobin (HbA_1c) and the fluctuation of blood sugar after meals. 

Differences between acarbose, voglibose and migliitol.

The biggest difference between them is that they inhibit different carbohydrases. 

• Acarbose has the effect of inhibition mainly to glucoamylase, sucrase and pancreatic α-amylase.
• Voglibose mainly has inhibitory effects on maltase and sucrase and the inhibitory activity of acarbose on these two enzymes is much lower than it. Voglibose does not inhibit amylase. The starch in the food will be decomposed into disaccharides in the small intestine and relatively small starch enter to the large intestine. Therefore, gastrointestinal reactions such as bloating are less likely to occur with voglibose.
• Miglitol can inhibit all α-glucosidases. Among them, it has the highest ability of inhibition to glucoamylase and sucrase. The reason may be because its structure is similar to glucose, so it can bind to various α-glucosidases.

Dosage of acarbose, voglibose and migliitol.

• Acarbose should be taken as a whole tablet immediately before a meal or chewed with the first few bites during a meal. Its starting dose is 50mg each time, 3 times a day. Then it was gradually increased to 100 mg each time, 3 times a day. In individual cases, it can be increased to 200 mg each time, 3 times a day.
• Voglibose needs to be taken before meals and have meals immediately after taken it. Adults usually take 3 times a day, 0.2mg each time. If the treatment effect is not obvious, it can be increased to 0.3mg each time after sufficient observation.
• Miglitol needs to be taken before meals and have meals immediately after taken it. Its starting dose is 25mg each time, 3 times a day. Then it was gradually increased to 100 mg each time, 3 times a day. The maximum dosage can be increased to 200 mg each time, 3 times a day.

Differences in hypoglycemic ability.

All α-glucosidases inhibitors can effectively reduce 2-hour postprandial blood glucose and HbA_1c levels in patients with type 2 diabetes. Studies have indicated that their HbA_1c-lowering efficiency is voglitose < miglitol < acarbose. 

Precautions.

Acarbose and voglibose can damage the liver and should not be used in patients with severe liver dysfunction. When the patient's glomerular filtration rate is greater than or equal to 25ml/min, no adjustment of dosage is required. However, when the patient's glomerular filtration rate is less than 25ml/min, it is contraindicated.

Miglitol is not metabolized by the liver, so no dose adjustment is required in patients with hepatic insufficiency. Most miglitol is excreted by the kidneys, so patients with renal impairment will accumulate it in the body. However, no dose adjustment is required in patients with mild to moderate renal insufficiency. It is not recommended for patients with severe renal insufficiency.

Common adverse reactions of α-glucosidase inhibitors.

The pharmacological effects of α-glucosidase inhibitors can cause gastrointestinal reactions. In theory, after α-glucosidase inhibitors works, all the sugar is absorbed before it reaches the terminal ileum. But in reality, undigested sugars and starches are broken down by enzymes in the large intestine. It produces acids such as lactic acid and acetic acid. As a result, the pH in the intestine will drop and the osmotic pressure will increase. It causes diarrhea. The decomposition reaction also produces gases such as hydrogen and carbon dioxide, which can cause bloating. Therefore, α-glucosidase inhibitors are recommended to start with small doses. Patients will generally gradually tolerate it after 2 weeks of treatment.

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Will metformin harm the liver and kidneys❓❓❓

Metformin was originally just a blood sugar lowering drug, but it was later
discovered to have many other effects, such as anti-aging, anti-cancer, etc., and it has been widely discussed (the medication should follow the doctor's guidelines and do not use it indiscriminately). Although with the advent of SGLT2 inhibitors, metformin has been replaced by SGLT2 inhibitors to a certain extent, metformin is still the drug of choice for type 2 diabetes in general. The vast majority of drugs will have some damage to the liver or kidneys. Many people would also think that metformin also harms the liver and kidneys. Will metformin harm the liver and kidneys?

Why do many people think that metformin harms the liver and kidneys?

In fact, the doctor prescribes oral hypoglycemic drugs for a newly diagnosed type 2 diabetes patient. According to the guidelines, if there are no contraindications, metformin should be recommended first. At this time, the doctor will ask the patient if he has any problems with the liver and kidney function, and may even check the liver and kidney function. As a result, many patients think that metformin will harm the liver and kidneys, so doctors will ask about their liver and kidney function. Of course, the doctor will explain to the patient that it is not that metformin hurts the liver and kidneys, but that patients with poor liver and kidney function may not be suitable for this medicine. However, doctors often do not have much time to explain the reasons to patients in detail, and most patients often fail to understand this highly specialized content. Therefore, patients will only remember the first impression that metformin may harm liver and kidney function. Then pass on the impression they remembered to others.

Why do doctors ask about liver and kidney function?

In fact, metformin neither hurts the liver nor the kidneys, and even some studies have shown that metformin can improve the liver and kidney function of some patients in some cases. So, why should doctors pay special attention to the patient's liver and kidney function when prescribing metformin? 

• Renal function: Metformin is mainly excreted from urine in its original form and cleared quickly. Therefore, metformin itself does not damage the kidneys. Since the launch of metformin, a large number of clinical and practical data accumulated in the past 100 years have also proved this point. Therefore, metformin does not harm the kidneys. However, in patients with renal insufficiency, the renal clearance of metformin decreases and the elimination half-life is prolonged, which leads to an increase in plasma metformin concentration and an increased risk of lactic acidosis. Therefore, patients with renal insufficiency need to adjust the dosage or discontinue according to the renal function when using metformin.
• Liver function: Metformin is not metabolized by the liver in the body, nor degraded in the body, and does not require liver detoxification, so it will not increase the burden on the liver, and it has no liver toxicity. It will not cause liver damage when used within the recommended dose. Therefore, metformin does not hurt the liver. The reason why doctors ask about liver function before prescribing metformin is that severely impaired liver function will significantly limit the patient's liver's ability to clear lactic acid. Therefore, the guidelines recommend that serum transaminase exceeds 3 times the upper limit of normal or severe liver insufficiency Of patients should avoid the use of metformin. 

Therefore, it is not that metformin harms liver and kidney function, but that the patient's existing liver and kidney function problems may affect the use of metformin.

Can't you take metformin if you have problems with liver and kidney function?

Not all patients with liver and kidney problems cannot use metformin. For example, for patients with type 2 diabetes who have normal renal function but have a small or large amount of albuminuria, metformin is still the first choice. For another example, patients with type 2 diabetes with hepatitis B or cirrhosis can also take metformin if they do not have severe liver insufficiency. However, it needs to be used under the guidance of a doctor, and follow the doctor's advice for regular liver and kidney function monitoring. Metformin has more than 60 years of global clinical application experience and its safety has been fully tested. Years of clinical studies have fully confirmed that metformin has a strong anti-diabetic effect, weight loss, cardiovascular protection, blood lipid improvement, tumor risk reduction, anti-aging, anti-inflammatory, improved intestinal flora, safety and tolerance, and high cost-benefit ratio and other advantages. This also makes metformin widely used by doctors. 

Metformin does not increase the risk of hypoglycemia when used alone, and it does not harm the liver or the kidneys. Long-term use does not increase the risk of hyperlactic acidemia or lactic acidosis. A common side effect of metformin is gastrointestinal discomfort. Metformin sustained-release tablets can solve this problem well.

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The difference between empagliflozin, dapagliflozin, canagliflozin and ertugliflozin. 😵😵😵

Nowadays, the pros and cons of hypoglycemic drugs are no longer based on the hypoglycemic value as an evaluation criterion, but whether they have heart and kidney protection while reducing blood glucose as the evaluation criterion. SGLT2 inhibitors are a new type of oral hypoglycemic drugs that have received great attention in recent years. In addition to the treatment of type 2 diabetes, it is also used for the treatment of chronic heart failure and chronic kidney disease. Empagliflozin, dapagliflozin, canagliflozin and ertugliflozin are very commonly used SGLT2 inhibitors. What is the difference between them?

1. Hypoglycemic mechanism.

The full name of SGLT2 inhibitors is sodium-glucose cotransporter 2 inhibitor. Normally, the glucose filtered through the glomerulus per day is about 180g/d, but all glucose will be reabsorbed by the sodium-glucose cotransporter (SGLT1, SGLT2) on the renal tubules. SGLT2 inhibitors reduce the reabsorption of glucose and sodium by the kidneys by inhibiting SGLT2. It can excrete 70~80g/d glucose from the urine, thereby exerting a hypoglycemic effect, and has a certain hypotensive effect. 

2. Other effects.

SGLT2 inhibitors can reduce glycosylated hemoglobin (HbA1c) 0.5-1.2%, weight 0.6-3.0kg, systolic blood pressure 3-5mmHg, and blood uric acid about 50μmol/L. They are all good for heart failure. SGLT2 inhibitors have shown cardiovascular and renal benefits in a series of large cardiovascular and renal outcomes studies. Among them, only empagliflozin and canagliflozin are beneficial to atherosclerotic vascular disease. Empagliflozin, canagliflozin and dapagliflozin are beneficial for delaying chronic kidney disease.

3. Clinical application.

The 2022 edition of "ADA Diabetes Medical Diagnosis and Treatment Standards" recommends:

For patients with atherosclerotic vascular disease, heart failure and/or diabetic kidney disease, it is recommended to use GLP-1 receptor agonists or SGLT-2 inhibitors as the initial treatment. According to the patient's blood sugar status, metformin is combined or not combined.

ASCVD/high-risk factors: It is recommended to use GLP-1 receptor agonist or SGLT2 inhibitor. Choose GLP-1 receptor agonists that have proven cardiovascular benefits: dulaglutide, liraglutide and semaglutide. Choose SGLT2 inhibitors that have proven cardiovascular benefits: empagliflozin and canagliflozin.

Heart failure: It is recommended to choose SGLT2 inhibitors that have been proven to be beneficial for heart failure: empagliflozin, canagliflozin, dapagliflozin and ertugliflozin.

Chronic kidney disease: 

Patients with chronic kidney disease and proteinuria should first choose SGLT2 inhibitors that can delay the progression of chronic kidney disease: canagliflozin, empagliflozin and dapagliflozin. If SGLT2 inhibitors are contraindicated/intolerant, choose GLP1 receptor agonists with cardiovascular benefits: dulaglutide, liraglutide and semaglutide. 

Patients with chronic kidney disease who do not have proteinuria should choose GLP-1 receptor agonists or SGLT2 inhibitors that have cardiovascular benefits.

4. Dosage.

SGLT2 inhibitor has diuretic effect. To avoid excessive nocturia, it is recommended to take it in the morning. They are not affected by meals.

Empagliflozin: It has a peak time of 1.5 hours and a half-life of 12.4 hours. Its recommended dosage is 10 mg once a day. The maximum dose is 25 mg once a day.

Dapagliflozin: It has a peak time of 2 hours and a half-life of 12.9 hours. Its recommended dosage is 5 mg once a day. The maximum dose is 10 mg once a day.

Canagliflozin: It has a peak time of 1-2 hours and a half-life of 10.6-13.1 hours. Its recommended dosage is 100 mg once a day. The maximum dose is 300 mg once a day.

Ertugliflozin: It has a peak time of 1 hours and a half-life of 16.6 hours. Its recommended dosage is 5 mg once a day.

5. Adverse effects.

Urinary and reproductive tract infections: SGLT2 inhibitors play a hypoglycemic effect mainly by promoting urinary glucose excretion. Due to the increased concentration of glucose in urine, SGLT2 inhibitors can significantly increase the risk of urinary tract infections and genital fungal infections. During the medication, you should increase the amount of drinking water and keep the vulva clean. If urinary tract infections and reproductive tract infections occur, symptomatic treatments such as antibacterial drugs (including antifungal drugs) are required.

Hypovolemia: SGLT2 inhibitors have an osmotic diuretic effect, which can lead to a decrease in blood volume. Elderly patients or those taking loop diuretics (such as furosemide) are at increased risk of hypovolemia. The main manifestations of hypovolemia are dehydration, orthostatic hypotension or hypotension.

Fracture risk: Patients with type 2 diabetes are more likely to fracture than the general population. The main fracture sites are the hip, foot and proximal femur. SGLT inhibitors can inhibit the reabsorption of sodium in the renal tubules and increase the reabsorption of phosphorus. This leads to increased blood phosphorus levels, stimulates parathyroid hormone secretion, and increases bone resorption. Canagliflozin can increase the risk of fractures.

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Summarize the diabetes medical diagnosis and treatment standards issued by the American Diabetes Association in 2022.👀

Recently, the American Diabetes Association released the Diabetes Medical Diagnosis and Treatment Standards for 2022. With regard to the treatment of type 2 diabetes, the new version of the guidelines has made many updates, weakening the status of metformin as the first-line medication.

1. Recommendations for the treatment of type 2 diabetes.

Initial treatment: Metformin is generally used. For patients with atherosclerotic cardiovascular disease (ASCVD)/high-risk factors, heart failure and/or chronic kidney disease, GLP-1 receptor agonist or SGLT2 inhibitor is recommended as the initial treatment. According to the patient's blood sugar status, metformin is combined or not combined. Unless the patient is contraindicated or intolerant, metformin should be continued after the initial insulin therapy to continuously improve blood sugar and metabolism. 

• Compared with insulin monotherapy, metformin combined with insulin can further reduce HbA1c, reduce insulin dosage, weight gain and the risk of hypoglycemia.

For some patients, early combination therapy can be considered when starting treatment to prolong the time of treatment failure. 

When choosing hypoglycemic drugs, cardiovascular complications, the efficacy of hypoglycemic drugs, the risk of hypoglycemia, the impact on weight, cost, availability, side effects and patient wishes should be considered.

Regardless of whether the HbA1c level is up to standard, if the patient has ASCVD/high-risk factors, kidney disease or heart failure, it is recommended to use SGLT2 inhibitors and/or GLP-1 receptor agonists that have proven cardiovascular benefits.

For patients with type 2 diabetes, GLP-1 receptor agonists are better than insulin.

If insulin is used, it is recommended to combine therapy with GLP-1 receptor agonists to improve the efficacy and durability of the therapeutic effect.

Patients with type 2 diabetes who are not up to the standard should be intensively treated as soon as possible.

The treatment plan should be re-evaluated every 3-6 months, and adjusted according to needs and new influencing factors.

Clinicians should be alert to insulin overtreatment. The following conditions may indicate that there may be excessive insulin consumption. Including the basic dose of more than 0.5IU/kg, the great difference in blood glucose between bedtime and fasting or before and after meals, hypoglycemia (symptomatic or asymptomatic), and high variability. When insulin overtreatment occurs, the next step of individualized treatment should be redesigned.

2. The choice of hypoglycemic drugs for patients with ASCVD, heart failure and chronic kidney disease.

ASCVD/high-risk factors: It is recommended to use GLP-1 receptor agonist or SGLT2 inhibitor. Choose GLP-1 receptor agonists that have proven cardiovascular benefits: dulaglutide, liraglutide and semaglutide. Choose SGLT2 inhibitors that have proven cardiovascular benefits: empagliflozin and canagliflozin.

Heart failure: It is recommended to choose SGLT2 inhibitors that have been proven to be beneficial for heart failure: empagliflozin, canagliflozin, dapagliflozin and ertugliflozin.

Chronic kidney disease: 

• Patients with chronic kidney disease and proteinuria should first choose SGLT2 inhibitors that can delay the progression of chronic kidney disease: canagliflozin, empagliflozin and dapagliflozin. If SGLT2 inhibitors are contraindicated/intolerant, choose GLP1 receptor agonists with cardiovascular benefits: dulaglutide, liraglutide and semaglutide. 
• Patients with chronic kidney disease who do not have proteinuria should choose GLP-1 receptor agonists or SGLT2 inhibitors that have cardiovascular benefits.

3. The main features of hypoglycemic drugs.

Metformin: It has a higher efficacy, no risk of hypoglycemia, and does not have much effect on body weight. There are potential benefits for cardiovascular, but no obvious benefits for the progression of kidney disease and heart failure.

SGLT2 inhibitor: It has a moderate effect, has no risk of hypoglycemia, and can reduce weight. Empagliflozin and canagliflozin have cardiovascular benefits. Empagliflozin, canagliflozin, dapagliflozin and ertugliflozin are beneficial for heart failure. Canagliflozin, dapagliflozin and empagliflozin are beneficial to the progression of kidney disease.

GLP-1 receptor agonist: It has higher efficacy, no risk of hypoglycemia, and can reduce weight. Dulaglutide, liraglutide, and semaglutide have cardiovascular benefits. Neutral to heart failure. Dulaglutide, liraglutide and semaglutide are beneficial for renal endpoints.

DPP-4 inhibitor: It has moderate efficacy, no risk of hypoglycemia, and does not affect body weight. There is no benefit to cardiovascular and the progression of kidney disease. In addition, saxagliptin has a potential risk of heart failure.

Thiazolidinedione: It has a higher efficacy, no risk of hypoglycemia, and will increase weight. Pioglitazone has potential cardiovascular benefits. Thiazolidinediones increase the risk of heart failure and are not beneficial to the progression of kidney disease.

Sulfonylureas: It has a higher efficacy. It has a risk of hypoglycemia and can increase weight. It has no effect on cardiovascular, heart failure and the progression of kidney disease.

Insulin: It has a higher efficacy. It has a risk of hypoglycemia and can increase weight. It has no effect on cardiovascular, heart failure and the progression of kidney disease.

4. Adverse reactions and precautions.

Metformin: Common gastrointestinal reactions (diarrhea, nausea). It may cause vitamin B12 deficiency.

SGLT2 inhibitor: SGLT2 inhibitors need to be stopped before any elective surgery to avoid the risk of DKA (diabetic ketoacidosis). Common side effects include genitourinary system infection, hypovolemia, risk of hypotension, elevated LDL-C, and Fournier gangrene. Canagliflozin has a risk of fracture.

GLP-1 receptor agonist: Common side effects are gastrointestinal reactions (nausea, vomiting, diarrhea). FDA black box warning: risk of thyroid C-cell tumors in rodent studies. However, the relevance to humans is not clear (liraglutide, dulaglutide, exenatide sustained-release agent, semaglutide).

DPP-4 inhibitor: Clinical trials have reported pancreatitis, but the causality has not yet been clarified. If pancreatitis is suspected, the drug should be discontinued. Joint pain is also a common side effect.

Thiazolidinedione: Common side effects include water and sodium retention (edema, heart failure) and the risk of fractures. Pioglitazone and rosiglitazone are at risk of congestive heart failure. Pioglitazone has a risk of bladder cancer. Rosiglitazone may increase LDL-C.

Sulfonylureas: The first generation of sulfonylureas (tolbutamide) has an increased risk of cardiovascular death.

Insulin: Risk of hypoglycemia: human insulin> human insulin analogues.

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Why is fasting blood sugar always unstable❓❓❓

Diabetes is a group of metabolic diseases characterized by hyperglycemia. Hyperglycemia is caused by defective insulin secretion or impaired biological effects, or both. Long-term high blood sugar causes chronic damage and dysfunction of various tissues, especially kidneys, blood vessels, heart, eyes and nerves. As a diabetic patient, in addition to using hypoglycemic drugs to control blood sugar, the patient must also monitor and record his blood sugar level. But why the fasting blood sugar of some patients have been sometimes high and sometimes low and they are always unstable, although they have the regular life, medication, diet and exercise arrangements?

Many people misunderstand that blood glucose before breakfast is equaled to fasting blood glucose.

Monitoring intravenous blood glucose in the hospital alone is not enough to understand the patient's condition changes. The doctors cannot formulate a reasonable and effective treatment plan based on that. Therefore, patients need to monitor blood glucose daily at home. 

After many people get up every morning, they usually finish the housework such as brushing their teeth and washing their face, making breakfast, or taking care of the children, and then measure their blood sugar. Many people mistakenly think that fasting blood glucose is the blood glucose level measured after getting up in the morning and taking blood before eating breakfast. In fact, it is not.

The correct meaning of fasting blood sugar.

After a person wakes up, the body will also be in a state of preparation for activity as the brain is awake. The levels of various hormones in the body begin to actively change and the blood sugar level also changes. Especially in patients treated with insulin, the blood sugar level is more likely to rise suddenly and decline suddenly.

In fact, fasting blood sugar is not measured the blood sugar on an empty stomach only. Fasting refers to the blood glucose level measured overnight, fasting for at least 8 hours and immediately after waking up. It can reflect the function of pancreatic islet β cells and generally indicates the secretion function of basic insulin. It is the most commonly used indicator for the detection of diabetes. The normal value should be less than 100mg/dl. If it is between 100-125mg/dl, it is pre-diabetes. If it is above 126mg/dl, it is diabetes.

Therefore, the first thing a diabetic patient should do after waking up is to wash his hands with warm water and then immediately check and record blood sugar. In this way, the fasting blood glucose can be measured accurately. If the fasting blood glucose is measured and there is still some time before breakfast, you can also compare the daily morning fasting blood glucose with the results of the pre-breakfast blood glucose measurement. It can provide a reference for adjusting medication in the future.

Why do the blood sugar before breakfast still need to measure even if the fasting blood glucose was measured?

The patient measures the pre-meal blood sugar can understand the blood sugar changes between meals. Without changing the dosage of drugs, the patient can rely on adjusting the type of food and the amount of food that he eat to ensure a stable blood sugar after a meal.

👉Only by accurately detecting blood sugar, the doctors can adjust the patient's medications and living habits reasonably and accurately. It also can help patients find problems at any time and go to the hospital for medical treatment in time. Accurate blood sugar testing can reduce the risk of diabetes complications. Good blood sugar control can improve the quality of life of patients and improve their physical condition.

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Drinking 100 ml of sugared beverages a day can increase the risk of cancer by 18%!!😱😱😱

Whenever you see a attractive beverage on the supermarket shelves, do you always want to drink a bottle and make yourself happy all day? In fact, the sugar in the drink has sneaked into your body at this time. If you don't control drinking, you may become a high sugar intake group unknowingly. 

So, what exactly is high sugar intake? High sugar intake refers to high added sugar intake. Added sugars include sucrose, sweeteners, honey and fruit juice, which are extracted and refined and added to foods or beverages to improve taste.

Will high sugar intake release "happiness factors" and relieve stress?

The intake of sugar will stimulate our brain to secrete dopamine. Dopamine is a kind of nerve substance that transmits excitement and happiness. It can make people feel happy. Therefore eating sugar can really make people happy and relieve stress.

What are the hazards of high sugar intake to the body?

Short term: High sugar intake will increase systemic inflammation and increase the risk of acne. This is why some people start to get acne after eating a lot of sweets.

Long term: Long-term high sugar intake will increase the risk of dental caries. Studies have found that 3 cups of sugared beverages a day will double the risk of dental caries. The effect of sugar to dental caries is not limited to modern times. In fact, as early as 500 years ago, excessive sugar consumption caused European aristocrats to have dental caries.

High sugar intake will also increase the risk of obesity. It is because added sugar is an "empty calorie food (most calorie and less nutrient in the food)". You are already full but you can still continue to enjoy a dessert after a meal. This is how sugar affects the satiety. Therefore, it is easy to eat too much sugar, which leads to excessive calorie intake and leads to obesity. In addition, high sugar intake can also increase the risk of diabetes. Added sugar can be quickly absorbed by the body and has a great impact on blood sugar fluctuations. Studies have shown that people who consume a lot of sugared beverages have an 18% increase in the risk of type 2 diabetes. 

Why does high sugar intake increase the risk of cancer?

In 2019, a study of more than 100,000 people showed that drinking 100 ml of sugared beverages a day would increase the overall risk of cancer by 18%. The researchers proposed some possible explanations for these results. It was including the effect of sugar in sugared beverages on visceral fat, blood sugar levels and inflammatory. All are associated with increased cancer risk. Long-term high sugar intake can lead to obesity and insulin resistance. It is resulting in oxidative stress, endocrine disorders and immune dysfunction in the body and leading to an increased risk of tumors.

After the tumor has occurred, the cancer cells will use the anaerobic glycolysis as the main energy supply method. So ordinary people and tumor patients both should control the intake of added sugar.

How to reduce sugar intake?

The World Cancer Research Fund (WCRF) and the American Cancer Institute (AICR) put forward the top ten recommendations for cancer prevention which include "limit the intake of sugared beverages."

We must learn to say goodbye to sweetness, reduce the intake of disserts and sweet drinks, eat more complex carbohydrates (coarse grains), drink more boiled water, lemonade or soda water.

Learn to look at the nutrient composition table on the food packaging to find out the hidden sugar.

If you really want to eat something sweet, we can choose fruit. While providing sweetness, it also provides vitamins, minerals and dietary fiber that are beneficial to health. 100% fruit juice is also a sugared beverage, so it is not recommended to use fruit juice instead of fruit. We can also choose suitable sugar substitute products and see if there are low-sugar/no-sugar products as alternatives when purchasing.

Try to reduce sugar intake, keep you healthy.👍

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Use body signals to alert for diabetes complications👴👵

Diabetes is a chronic metabolic disorder based on genetics and the environment, which can cause damage to capillaries, large blood vessels, eyes, feet, heart, brain and other organs. The patient will produce some corresponding symptoms due to persistent hyperglycemia. If doctors and patients can recognize these changes early and intervene in time. It can effectively delay the development of diabetes to a more severe degree.

1. Skin: Abnormal sweat secretion and pigmentation

Skin lesions can occur in the skin of the whole body and occurring in various periods of diabetes. It is manifested as hyperhidrosis on the trunk, less sweat on the limbs, dry skin and itching, cracked hands and feet, erythema on the anterior tibia of the calf, and gradually progressing to a circular pigmented area (anterior tibial spot).
Mechanism: Autonomic nerves can not regulate sweat glands normally. It result in abnormal sweat gland secretion. Coupled with long-term metabolic disorders, it causes neuropathy, microvascular disease, arteriosclerosis and skin infections, which in turn leads to skin lesions.

2. Eyes: pain and blurred vision

Diabetic retinopathy can cause blurred vision, decreased vision. Some patients may have color recognition disorders or eye pain.
Mechanism: Eye basement membrane thickened, capillary capillaries, and impaired blood retinal barrier function caused abnormal penetration. It would lead to retinal edema and the formation of new blood vessels over a period time.

3. Oral: periodontal abscess and periodontitis

Patients with poor blood sugar control lead to severe inflammation of the periodontal tissue, red and swollen gingival margins can be granulomatous hyperplasia, easy to bleed, periodontal pockets often have pus and periodontal abscesses. In severe cases, multiple periodontal abscesses and rapid destruction of alveolar bone can occur.
Mechanism: Diabetes and periodontitis affect each other. The high-sugar environment of diabetic patients will cause the microbes grow rapidly in the oral and causing a variety of oral diseases. The failure of effective control of oral diseases will further worsen the condition of diabetes.

4. Foot: infection and ulceration

Diabetic feet are manifested by infections of varying severity, ulcers, neurological disorders, damage or lesion of soft tissues and bones and joints of the foot. Severe cases may require amputation. The probability of foot ulceration or necrosis in diabetic patients is 20~30%.
Mechanism: Diabetic foot is caused by peripheral neuropathy, infection and vascular stenosis or occlusion.

5. Bone: bone pain and osteoporosis

Diabetes combined with osteoporosis will cause bone pains. Convulsions of the limbs may occur due to increased urinary calcium excretion. People with severe osteoporosis are prone to fractures. If there is a significant compression fracture of the spine, there will be a hunchback, height shorter and a reduction in the distance between the costal margin and the iliac ridge.
Mechanism: Poor blood sugar controlling caused increaseing urinary sugar excretion, a large loss of blood calcium with urine, inhibition of bone formation, bone transformation at a low level. The end products of glycosylation may increase bone fragility.

6. Joints: pain and limited mobility

It shows joint pain, swelling, tenderness, joint morning stiffness, rub of joint and limited joint movement.
Mechanism: Diabetes can cause joint neuropathy. It result in vascular nutritional dysfunction, hypoesthesia, bone destruction, articular cartilage damage and even fractures.

7. Lower limbs: pain and numbness

Diabetes more than 10 years are prone to obvious peripheral neuropathy. The clinical manifestations are pain, numbness, burning or needle sensation in the limbs. The symptoms are often bilaterally symmetrical and are more obvious at the ends of the hands and feet. Severe pain at the proximal end of one lower extremity is more common and it can be involved with both distal motor nerves at the same time. It accompanied by rapidly progressing muscle weakness and muscle atrophy.
Mechanism: The risk of occurrence is related to factors such as the level of blood sugar control and the course of diabetes. The occurrence of pathology involves multiple mechanisms such as oxidative stress, polyols and microcirculation disorders.

8. Gastrointestinal: hiccups, diarrhea and constipation

Patients will have stomach symptoms such as hiccups, dysphagia, stomach upset, full upper abdomen, constipation, diarrhea and bowel disorders.
Mechanism: Diabetic autonomic neuropathy can manifest in multiple systems of the human body and then appear corresponding symptoms.

9. Urine: special smell and foamy urine

There is an increase in foam in the urine which looks like beer foam. The urine appears a special smell, frequent and incomplete urination.
Mechanism: Foamy urine is due to increased urine albumin excretion. It results in increased urine tension and foam. The special smell in urine is due to the increased amount of ketones produced by the body under the influence of high blood sugar. It is always seen in diabetic ketosis or ketoacidosis.

10. Cardiovascular: syncope and orthostatic hypotension

It manifests as syncope, orthostatic hypotension, painless myocardial infarction, abnormal coronary systolic function, cardiac arrest or sudden death.
Mechanism: Diabetes is a cardiovascular complication caused by increased blood sugar and blood lipids. High blood pressure and lipid and calcium deposits in the coronary arteries of the heart. These make hardening and stenosis of the arteries.

11. Peripheral large blood vessels: cold skin and walking weakness

The pulsation of the dorsal artery of the foot disappeared, the skin of the lower extremities was cold and the walking fatigue disappeared after 2 to 3 minutes of rest. Then the calf pain during walking may appear which relieved after rest.
Mechanism: Diabetes leads to peripheral vascular disease which is stenosis and occlusion of blood vessels except coronary arteries and cerebral blood vessels. There are corresponding ischemic spasm or necrosis of distal tissues. It is mainly involving lower extremity arteries.

12. Sexual dysfunction

Men are manifested as retrograde ejaculation, erectile dysfunction, delayed ejaculation, premature ejaculation, non-ejaculation and so on. Women present with symptoms such as decreased vaginal lubrication, low libido, female orgasm disorders and dyspareunia.
Mechanism: In men, erectile and ejaculation disorders are caused by autonomic nervous diseases. Erectile disorders are caused by vascular diseases. In women, because women are in a state of chronic hyperglycemia, antioxidant defense effectiveness is reduced. It is leading to aggravation of the disease and various sexual dysfunctions.

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Inventory of various new discoveries of metformin😎😎😎

Metformin is an anti-diabetic drug and a classic oral hypoglycemic agent. Since its inception in 1957, it has been used clinically for more than 60 years. It is currently one of the most widely used oral hypoglycemic drugs in the world. Even though there are many new hypoglycemic drugs, metformin is still the primary drug for type 2 diabetes.

Metformin was born in 1929 and originated from galega officinalis. In 1957, French diabetologist professor Jean Sterne first used metformin for clinical hypoglycemic reduction. Then its application value is still being discovered. Let us take a look at what new discoveries have been made recently.

1. Cancer

Acidic phospholipids play an important role in regulating electrostatic membrane association of programmed cell death ligand 1 cytoplasmic domain (PD-L1-CD). Metformin can competitively dissociate PD-L1-CD from the membrane and affect the stability of PD-L1. This revealed that the molecular mechanism of metformin's anti-tumor effect and provided new ideas for related immunotherapy targeting PD-L1.

There are many studies that supporting metformin can decrease the risk or improve the symptoms of cancer patients. Such as esophageal squamous cell cancer, pancreatic cancer, primary bone cancer.

2. Obstetrics & Gynecology

a. Improve neonatal obesity

    Metformin has many benefits for mother's blood glucose and neonatal obesity, including improved blood glucose, reduced caesarean section, reduced mother's weight, lower insulin requirements,  lower birth weight and obesity measurements of newborns.

b. Prevent adverse pregnancy outcomes in patients with polycystic ovary syndrome

    Metformin can prevent late period abortion and premature birth in women with polycystic ovary syndrome.

3. Metabolic diseases

Metformin can improve the metabolic status of patients treated with systemic glucocorticoids. It can not only reverse the metabolic complications caused by the use of systemic glucocorticoids, but also reserve the anti-inflammatory effects of glucocorticoids. It benefits many patients taking systemic glucocorticoids.

4. Cardiovascular System

 a. Heart failure

    Non-diabetic heart failure patients with reduced ejection fraction (HFrEF) use metformin to reduce myocardial oxygen consumption and improve myocardial efficiency.

b. Left ventricular hypertrophy

    Metformin treatment significantly reduced the left ventricular mass index. Patients taking metformin reduced left ventricular thickening by two time less. In addition, metformin also reduced blood pressure, oxidative stress, and weight. Metformin has the potential to improve cardiovascular health.

c. Air-pollution-induced thrombosis

    Atmospheric particulate matter can induce alveolar macrophages to release pro-inflammatory factors including interleukin 6 (IL-6), leading to arterial thrombosis and death.

    Metformin blocks the mitochondrial electron transport and inhibits the production of reactive oxygen species, thereby blocking the release of IL-6 and inhibiting the formation of arterial thrombosis. This confirms that metformin can be used as a potential therapeutic drug to prevent cardiovascular diseases caused by air pollution.

5. Nervous system

a. Cognitive and nerve recovery after brain tumor surgery

    For children with brain tumor patients who have received craniocerebral radiotherapy, metformin can significantly improve their statement memory and working memory function, repairing white matter damage. Metformin is also safe and tolerable in this population.

b. Multiple Sclerosis

    After treatment with metformin, oligodendrocyte precursor cells can restore their response to the signal of promoting-differentiation, promote the regeneration of nerve myelin. This is useful for the treatment of central nerve demyelination such as multiple sclerosis.

c. Cognitive decline and dementia

    Patients with type 2 diabetes who take metformin have slower cognitive decline and a lower risk of dementia.

6. Locomotor system

a. Osteoarthritis

    Metformin can prevent the occurrence and development of osteoarthritis, alleviate the pain sensitivity associated with osteoarthritis in mice. Its protective effect on cartilage is mainly through the activation of AMPK signals.

b. Intervertebral disc degenerative disease

    Metformin can promote the release of small extracellular vesicles of mesenchymal stem cells, increase the level of proteins that regulate cell proliferation in the vesicles, and can optimize the application effect of extracellular vesicles in the regeneration and repair of intervertebral discs.

7. Digestive system

Metformin stimulates bile secretion in the intact liver, but this drug can also cause severe damage to bile acid secretion.

8. Infection

a. COVID-19

   Metformin inhibits the activation of NLRP3 inflammasomes and the production of IL-1β in cultured macrophages and alveolar macrophages, as well as the secretion of inflammasome-independent IL-6, thereby attenuating lipopolysaccharide and COVID-19 induced acute respiratory distress syndrome. Metformin can be a potential treatment for severely patients with COVID-19 and other induced acute respiratory distress syndrome.

b. HIV

    Metformin reacted on mitochondrial respiratory chain complex-I and inhibit the oxidative phosphorylation (OXPHOS) pathway. It inhibited the replication of human CD4⁺ T cells and HIV-1 virus in humanized mouse models. It revealed that metformin and others OXPHOS pathway inhibitors may be an adjunct to treat AIDS.

👉Metformin has also anti-aging effect. Most effects still are at the research stage and may not be used on treatment. Therefore, metformin still deserves more in depth research.

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What should you do if you forget to take your oral diabetes drug??😨😨

It is very common to see that the patient forget to take his diabetes drug. But what should you do if you forget to take it? Today will talk about that and how the medicine taken.

Metformin

General and sustained-release dosage form are taken during or after meal. Enteric-coated dosage form is taken before meals.

If you forget to take the medicine, take it as soon as possible. If the time is close to the next dose, do not take it and must not double the next dose!

Acarbose

Take the tablets with meal (chew together with the food and then swallow). Capsule form should be swallowed the whole immediately before meals. Do not take acarbose if you do not have a meal!!!

If you forget to take acarbose while eating, you can chew it during or immediately after the meal. If it is close to the next dose, do not take it and must not double the next dose!

Gliclazide sustained-release tablets / Glipizide controlled-release tablets

Take it before breakfast. If you haven't breakfast, take the medicine before the first meal.

If you forget to take the medicine before breakfast, you can take it during or immediately after breakfast.  If it is close to the next dose, do not take it and must not double the next dose!

Nateglinide / Repaglinide

Take the medicine immediately before meal. Do not take medicine if you do not have a meal.

If you forget to take the medicine before a meal, you can take it immediately during or after a meal. If it is close to the next dose, do not take it and must not double the next dose!

Rosiglitazone Tablets / Pioglitazone Dispersible Tablets

Take the medicine before or after meal. 

If you forget to take the medicine, take it as soon as possible. If it is close to the next dose, do not take it and must not double the next dose!

Sitagliptin / Saxagliptin / Alogliptin / Vildagliptin / Linagliptin

These medicines are not affected by food. They can be taken with or without food

If you forget to take the medicine, take it as soon as possible. If it is close to the next dose, do not take it and must not double the next dose!

Dapagliflozin

Take medicine in the morning. Can be taken with or without food. 

If you forget to take the medicine, take it as soon as possible. If it is close to the next dose, do not take it and must not double the next dose!

Canagliflozin

Take it before the first meal every day.

If you forget to take the medicine, take it as soon as possible. If it is close to the next dose, do not take it and must not double the next dose!

***Summary, metformin and acarbose will irritate intestine, so they should be taken during or after meal. And if you forget to take your diabetes drugs, take it as soon as possible. But if the time is close to the next dose, just take the next dose and must not double the dose!!!!!

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What fruits can the diabetes patients eat?😋

Diet is a very important part to patients with diabetes mellitus. That is easy to confusing about what fruits they are able to eat. Today, let's simply go though about the blood glucose influence of fruits.

1. Glycemic Index (GI) and Glycemic Load (GL)

Glycemic Index (GI) and Glycemic Load (GL) are two numbers that can be refer to the food whether be able to eat by the diabetes patients.

GI is a number of increasing blood glucose after eating 50g of carbohydrate foods 2 hours. The range is 0-100. GI>70 is high GI food, the patients should avoid to eat them. GI is 55-70, patients can eat a limit number. And GI<55 is low GI, patients are able to eat.

GI only can show the "quality" of carbohydrate foods. GL can show the "quantity". GL=GI x The amount of carbohydrate per 1g of food. GL>20 is high GL food, GL=10-20 is medium GL food, and GL<10 is low GL food.

2. The GI and GL of some fruits

Name	GI	Carbohydrate	GL
Papaya	25	7.2	1.8
Strawberry	29	7.1	2.1
Lemon	34	6.2	2.1
Cherry	22	10.2	2.2
Peach	28	10.1	2.8
Dragon Fruit	25	13.3	3.3
Citrus	43	10.2	4.4
Orange	43	11.1	4.8
Apple	36	13.7	4.9
Watermelon	72	6.8	4.9
Cantaloupe	70	7.9	5.5
Pineapple	66	10.8	7.1
Mango	55	12.9	7.1
Kiwifruit	52	14.5	7.5
Banana	52	20.8	10.8
Coconut	40	31.3	12.5

Green: Can be eaten in moderation. Yellow: Limited consumption. Red: Not recommended eaten.

👀This above content is only for reference, please consult your doctor for more details.

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