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Rewinding the clock on aging blood vesselsEnhance insulin sensitivity and promote longevity -
Insulin resistance, a condition in which your cells stop responding properly to insulin, is incredibly common. In fact, the prevalence of insulin resistance is However, certain dietary and lifestyle habits can dramatically improve or help prevent this condition.
Insulin is a hormone that your pancreas secretes. It regulates the amounts of nutrients circulating in your bloodstream 2.
Although insulin is mostly involved in blood sugar regulation, it also affects fat and protein metabolism 2. When you eat a meal that contains carbs , the amount of sugar in your bloodstream increases. The cells in your pancreas sense this increase and release insulin into your blood.
Insulin then travels around your bloodstream, telling your cells to pick up sugar from your blood. This process helps regulate blood sugar levels and prevent high blood sugar, which can have harmful effects if left untreated 3 , 4.
However, cells sometimes stop responding to insulin correctly. This is called insulin resistance. When you have this condition, your pancreas produces even more insulin to lower your blood sugar levels.
This leads to high insulin levels in your blood, known as hyperinsulinemia 5. Over time, your cells may become increasingly resistant to insulin, resulting in a rise in both insulin and blood sugar levels.
If your blood sugar levels exceed a certain threshold, you may receive a diagnosis of type 2 diabetes. If you have insulin resistance, you have low insulin sensitivity. Conversely, if you are sensitive to insulin, you have low insulin resistance 7.
Insulin resistance occurs when your cells stop responding to the hormone insulin. This causes higher insulin and blood sugar levels, potentially leading to type 2 diabetes. One possible cause is increased levels of free fatty acids in your blood, which can cause cells to stop responding properly to insulin 8.
The main causes of elevated free fatty acids are consumption of too many calories and the presence of excess body fat. In fact, overeating, weight gain , and obesity are all strongly associated with insulin resistance 9 , 10 , Visceral fat, the harmful belly fat that can accumulate around your organs, may release many free fatty acids into your blood, as well as inflammatory hormones that drive insulin resistance 12 , Although insulin resistance is more common among people with overweight or obesity, anyone can develop it Black, Hispanic, and Asian individuals are at particularly high risk The main causes of insulin resistance are overeating and increased body fat, especially in the belly area.
Other factors that can contribute include high sugar intake, inflammation, inactivity, and genetics. A healthcare professional can use several methods to determine whether you have insulin resistance. For example, high fasting insulin levels are a strong indicator of this condition A fairly accurate test called HOMA-IR can estimate insulin resistance based on your blood sugar and insulin levels There are also ways to measure blood sugar regulation more directly, such as an oral glucose tolerance test — but this takes several hours.
Your risk of insulin resistance increases greatly if you have overweight or obesity, especially if you have large amounts of belly fat 7. A skin condition called acanthosis nigricans, which causes dark spots on your skin, can also indicate insulin resistance Low HDL good cholesterol levels and high blood triglycerides are two other markers strongly associated with insulin resistance High insulin and blood sugar levels are key symptoms of insulin resistance.
For the positive, the intake of BCAAs can improve the function of muscle and heart, reduce the inflammation of liver and kidney, and enhance intestinal metabolism. Moreover, increased endogenous BCAAs caused by BCAT-1 gene silence and increased leukocyte telomere length can also have a positive effect on longevity.
For the negative, the effects of BCAAs on insulin resistance, obesity, and T2DM indicate their negative influence on lifespan.
Furthermore, the molecular mechanism of BCAAs on shortened life is related to the autophagy induced by decreased TORC1, and the decreased cell proliferation induced by DNA damage. From the two sides, miR seems a potential regulatory target whose expression level is associated with lifespan through adjusting BCAAs catabolism.
High levels of BCAAs are often detected in the plasma of patients with T2DM and obese people 28 , However, considering the health benefits of BCAAs, the correlations between high levels of BCAAs and insulin resistance, obesity and T2DM seem contradictory.
The possible mechanism by which BCAAs negatively regulate lifespan is by reducing TORC1 activity, reducing the phosphorylation level of S6K S6 kinase , downregulating S6K mRNA translation, and inducing autophagy BCAAs are effective activators of the TOR signal, and S6K is a direct downstream target of this signal.
Research results show that overexpression of ARGK-1 can extend the life of C. Studies on rapamycin-induced Drosophila autophagy 34 and dietary restriction-triggered C. elegans autophagy 35 have demonstrated that initiation of autophagy can lead to prolonged lifespan.
In addition, adverse effects of leucine, the main component of branched-chain amino acids, on longevity have been reported. Leucine can induce senescence of MC3T3-E1 cells through DNA damage, which has a negative effect on the proliferation of bone cells.
These results may provide new insights into previous studies on the supplementation of amino acids to promote bone health Depletion of leucine prolongs the life of leucine-auxotrophic cells, leading to cell senescence and cell cycle stagnation in the G1 phase, which are dependent on genes in the Ecl1 family These studies suggest that leucine, as one of the main components of BCAAs, may play an important role in the negative effects of aging.
In recent years, an increasing number of studies have begun to seek the best way to regulate lifespan through the study of branched-chain amino acid metabolism. Among them, BCAA catabolism regulated by miR is the best way to study the regulation of BCAAs on lifespan. Overexpression and inhibition of miR can shorten the lifespan, especially when consuming foods containing excessive protein.
Expression of miR reduced the metabolic capacity of BCAAs. The resulting increase in BCAA concentration may stimulate TOR kinase 38 , 39 , thereby shortening lifespan. Transgenic inhibition with the use of miRNA sponges also shortens the lifespan, especially on a protein-rich diet Changes in miRNA expression in adult Drosophila showed that miR was significantly downregulated in adult Drosophila, which was consistent with its effect on lifespan.
Therefore, optimal metabolic adaptation and optimal longevity effects seem to be achieved by regulating BCAA catabolism by miR Figure 2. In summary, the effects of BCAAs on longevity have many controversial consequences, and the possible mechanisms are complex. It is certain that the positive and negative regulation of BCAAs on longevity has a great relationship with the external environment, diseases and intake.
For example, supplementing BCAAs under specific dietary restrictions can improve metabolic health, improve glucose tolerance, and reduce fat accumulation 41 , while BCAAs in combination with a high-fat diet tend to lead to the development of obesity-related insulin resistance The regulatory mechanism of BCAAs on longevity may be related to the regulation by miR of BCAA catabolism.
Many studies have confirmed that BCAAs may play a causal role in the pathogenesis of type 2 diabetes 43 — 45 , and BCAAs contribute to the development of obesity-related insulin resistance in humans and rodents on a high-fat diet HFD Studies of male rats and humans have shown that high-level BCAA intake is associated with high fat intake, leading to insulin resistance and glucose intolerance, which ultimately result in metabolic syndrome 42 , In obese mice induced by a high-fat diet, BCAA supplementation exacerbated obesity-related hepatic glucose and lipid metabolism disorders by weakening Akt2 signaling, thereby causing severe hepatic metabolic disorders and hepatic insulin resistance Moreover, supplementation with BCAAs combined with a high-fat diet was associated with increased plasma BCAA concentrations in adult rats Moreover, reducing BCAAs in the diet in this situation moderately improves glucose tolerance and reduces fat mass increase Similarly, high BCAA levels in breast milk are associated with a high risk of insulin resistance in the children of obese women A maternal high-fat diet alone or supplemented with BCAAs can impair the glycemic control of these children in adulthood.
Male and female offspring fed high-fat diets containing BCAAs showed serious insulin intolerance and elevated fasting blood glucose levels, which might be related to the influence of the hypothalamic ER-α pathway In addition, daily intake of BCAAs, namely, leucine, isoleucine, and valine, by mothers with gestational diabetes may also increase the risk of overweight and insulin resistance in their children 7.
Other studies have not found an association between dietary BCAA intake and adult plasma BCAA concentrations 52 , In contrast, supplementing the maternal diet with BCAAs prevents age-related and diet-related insulin intolerance, thereby protecting offspring.
In healthy individuals, BCAAs appear to play beneficial roles, including reducing the risk of obesity, increasing muscle mass, potentially improving glucose sensitivity, and possibly exerting therapeutic effects in patients with cirrhosis and encephalopathy 54 — However, high levels of circulating BCAAs in serum or plasma are thought to be associated with obesity and insulin resistance Studies have shown that long-term exposure to high levels of BCAAs stimulates hyperlipidemia and obesity, which has a positive association with fasting glucose levels, LDL and triglyceride levels and a negative correlation with HDL-C and inhibits the TCA tricarboxylic acid cycle directly through BCKA accumulation 54 , 59 — When BCAA metabolic disorders occur, such as in metabolic syndrome, the catabolites of valine, isoleucine, and leucine may accumulate and produce negative metabolic effects.
Furthermore, the risk of developing T2DM increases because of the genetic predisposition to BCAA metabolism impairment Several studies have reported that plasma or serum BCAA levels can predict the development of T2DM BCAA metabolites are associated with the risk of obesity and insulin resistance.
However, it is unknown which BCAAs, that is, leucine, valine or isoleucine, influence insulin resistance. Moreover, the glucose tolerance and pyruvate tolerance of mice fed a low-leucine diet were significantly increased, indicating that leucine restriction could enhance gluconeogenesis Leucine can also regulate glucose uptake by L6 myotubes independent of the mTORc1 and AKT signaling pathways, and the concentration of leucine in the culture medium has a dose-dependent relationship with non-insulin-stimulated glucose uptake in cells Nevertheless, low concentrations of leucine did not change insulin signaling and were not associated with insulin resistance but increased the lipid content in myotubes A cohort study of women without prediabetes also showed that leucine supplementation had no effect on insulin sensitivity Recent studies have shown that valine supplementation alone has no effect on pAkt and Akt in myotubes and was not associated with insulin stimulation or different levels of insulin resistance However, valine in combination with leucine, isoleucine or protein can affect insulin signaling and related metabolic pathology.
Moreover, excessive intake of valine can independently induce insulin resistance. In animals, 3-HIB is secreted by muscle, which activates the transport of endothelial fatty acids, stimulates the uptake of muscle fatty acids, and promotes muscle lipid accumulation and insulin resistance 8.
The addition of 3-HIB to white and brown adipose cell cultures increased fatty acid uptake and regulated insulin-stimulated glucose uptake in a time-dependent manner In humans, 3-HIB has been shown to be associated with insulin resistance in subjects with diabetes and with insulin resistance in overweight and obese individuals It was shown that in a cohort of 4, men and women, cyclic 3-HIB increased with elevated levels of hyperglycemia and T2DM.
In addition, after weight loss, cyclic 3-HIB concentrations increase briefly and then decrease significantly. Studies of isoleucine have shown that it can significantly increase muscle and fat mass and cause insulin resistance.
Furthermore, it can also upregulate the levels of key lipogenic proteins and myogenic proteins. More importantly, through mitochondrial function lesions, isoleucine can harm the gastrocnemius and tibialis anterior and lead to cavitation, swelling, cristae fractures, etc.
In addition, isoleucine promotes myogenesis and increases lipid droplet accumulation in myotubes. In general, isoleucine can increase muscle mass and induce insulin resistance through myogenesis and intracellular lipid deposition Although most of the recent studies have confirmed that an appropriate supply of BCAAs to the normal body has no or a positive effect on insulin sensitivity, in the diabetic or obese body or in the case of an excessive supply of BCAAs to the normal body, BCAAs have negative effects on insulin sensitivity and sometimes can lead to insulin resistance.
At present, there are several speculations about the mechanism of this phenomenon: one is the catabolite of BCAAs, that is, branched-chain ketone acids BCKAs. The expression of BCAA catabolic enzymes in the hearts of fasting mice was decreased, and circulating BCKAs were increased, while BCAAs were not increased.
Similar increases in circulating BCKAs were associated with changes in BCAA catabolic enzyme expression in diet-induced obesity DIO mice. Exposure of muscle cells to high levels of BCKAs inhibits insulin-induced AKT phosphorylation and reduces glucose uptake and mitochondrial oxygen consumption.
Changes in the intracellular BCKA clearance rate by gene-regulated expression of BCKDK and BCKDHA have similar effects on AKT phosphorylation. Therefore, excessive amounts of BCKAs are the real cause of insulin resistance Second, it has been hypothesized that mammalian target of rapamycin complex 1 mTORC1 is overactivated in the presence of amino acid overload, leading to a reduction in insulin-stimulated glucose uptake, which is caused by insulin receptor substrate IRS degradation and reduced Akt-AS activity However, this hypothesis can only explain the negative effects of excessive intake of BCAAs but cannot explain the regulatory mechanism of insulin sensitivity by the addition of BCAAs in disease models.
Furthermore, the results still do not explain the findings on HMB the metabolite of leucine — hydroxy-p-methylbutyric acid , which is thought to reduce insulin resistance HMB may reduce insulin resistance and hepatic steatosis by inhibiting GLUT-2 in the liver of high-fat diet-fed rats For humans, acute HMB treatment improves insulin resistance after glucose loading in young men but has no effect on insulin sensitivity in older men The above phenomena are not consistent with the effect of leucine on insulin resistance, and there is no recent research on the mechanism of this contradiction, so the regulation of these phenomena requires further investigation.
The improvement in insulin resistance is associated with longevity. The metabolic traits in centenarians are maintaining insulin sensitivity and a lower incidence of diabetes 77 , which suggests that glucose homeostasis may play a crucial role in health and longevity.
At present, much of the increase in longevity and health is achieved by improving insulin sensitivity. New insights into certain features of vegetarianism suggest that vegetarianism can improve insulin resistance and dyslipidemia and related abnormalities by limiting proteins or certain amino acids leucine or methionine and has the potential to extend life Aging PASK-deletion mice exhibited overexpression of the longevity gene FoxO3a and a normal HOMA-IR index, which simultaneously confirmed that mice lacking PASK had better insulin sensitivity and glucose tolerance Drosophila melanogaster fed a high-sugar diet showed signs of insulin resistance and a reduced lifespan Moreover, in mice and humans, an increase in circulating BCAAs is associated with a high risk of insulin resistance and diabetes, as well as an increased mortality in mice Studies of calorie restriction CR have shown that eating high-calorie foods can impair metabolism and accelerate aging; in contrast, CR can prevent age-related metabolic diseases and extend life 81 , and the main mechanism by which calorie restriction prolongs life is to improve aging by enhancing insulin sensitivity 82 , 83 , which also suggests a positive correlation between increased longevity and insulin sensitivity.
In a study of mice fed a medium-fat or high-fat diet, it was observed that low insulin levels significantly increased lifespan, high insulin levels contributed to age-dependent insulin resistance, and decreased basal insulin levels could extend lifespan These results suggest that increased insulin levels and insulin sensitivity have a positive effect on longevity.
Although several studies have shown that improved insulin sensitivity promotes health and longevity, there is also clear evidence that insulin sensitivity is not necessarily related to healthy aging and may even be counterproductive.
In some insulin-related gene knockout mouse models, insulin resistance is induced in one or more tissues, and a significant increase in the lifespan of mice can be observed.
Female insulin receptor substrate IRS 1 knockout mice also showed signs of longevity Furthermore, rapamycin extended the lifespan of mice by inhibiting mTORC1 and impaired glucose homeostasis to induce insulin resistance by interfering with mTORC2 signaling S6K1 knockout female mice showed an extended lifespan and induced loss of insulin sensitivity Previous studies have focused on the positive and negative correlations between insulin resistance and lifespan, but recent findings suggest the more interesting possibility that insulin resistance or metabolic defects may be independent of longevity, which also explains the above two opposite results.
As insulin resistance is independent of lifespan, the opposite results of lifespan may be led by other different factors, and insulin resistance is not the main reason for lifespan-changing. From this study we could see that a high-sugar diet can shorten the lifespan of Drosophila, which could be saved by water supplementation.
In contrast, metabolic defects, which are widely thought to lead to reduced survival, have been shown to be unrelated to water. Drosophila that had been watered on a high-sugar diet still showed all the metabolic defects similar to diabetes and had the same survival rates as healthy controls, suggesting that obesity and insulin resistance by themselves did not shorten fly life.
The mechanism by which a high-sugar diet regulates lifespan in Drosophila is thought to be a water-dependent way of regulating uric acid production: the high-sugar diet promotes the accumulation of uric acid a final product of purine catabolism and enhances this process. Furthermore, this phenomenon is completely restored by water or allopurinol treatment Mice deficient in fatty acid binding protein FABP showed extended metabolic health cycles, which were protective against insulin resistance, glucose intolerance, inflammation, deterioration of adipose tissue integrity, and fatty liver disease.
However, the mice lacking FABP showed no signs of longevity. These data suggest that metabolic health in mice can be detached from longevity in the absence of caloric restriction, suggesting that these pathways may act independently 88 Figure 3.
Figure 3. The different relationship between insulin resistance and longevity. Insulin resistance in insulin-related gene IGF-1R, FIR, and IRS1 knockout mice is induced in one or more tissues and is accompanied by a significant extension of mouse lifespan.
On the other hand, Drosophila fed a high-sugar diet are characterized by insulin resistance and a shortened lifespan. Increased circulating BCAAs in mice lead to insulin resistance development and increased mortality in mice. Furthermore, calorie restriction CR can extend life by improving insulin sensitivity.
Moreover, the shortened lifespan caused by high sugar feeding in Drosophila can be saved by water, suggesting that insulin resistance may be independent of lifespan regulation. This review summarizes the contradictory role of branched-chain amino acids in lifespan and insulin resistance. In this review, we attempt to explain these conflicting findings from a physiological and pathological perspective and to draw conclusions about the possible regulatory mechanisms between BCAAs and aging, BCAAs and insulin resistance, and aging and insulin resistance.
When explaining the above arguments, it should be noted that 1 metabolic regulation of the body is very complex, and the existence of aging and insulin resistance may also have an impact on metabolism, including some compensatory effects; 2 the effects of BCAA supplementation on aging and insulin resistance should be comprehensively analyzed in combination with sex, age, dietary conditions and basic diseases; 3 at present, exogenous BCAAs are not well correlated with endogenous BCAA levels in plasma and serum; and 4 there are some great differences in diseases, aging, food intake and water intake, especially in animal models.
Therefore, BCAA-based research must refer to the basic survival data of the research subject for comprehensive analysis. Due to the complexity of metabolism and body responses, it is difficult to draw convincing conclusions about the effects of BCAAs on aging and insulin resistance. From the screening of the literature, the following possible regulatory mechanisms of BCAAs, aging and insulin resistance can be concluded: 1 Autophagy can significantly extend the lifespan of yeast, C.
elegans and mice. However, autophagy alone is neither sufficient to extend the lifespan nor necessary to extend the lifespan. In the absence of autophagy, the inhibition of protein synthesis in animals that were fed adequate food could extend life.
In summary, autophagy may have a specific regulatory mechanism to prolong life, and its specificity may be related to the environment of the food supply and the regulation and triggering of longevity pathways.
To some extent, this also explains the mechanism by which BCAAs and insulin resistance influence lifespan. However, there is currently no reliable study on the triggering mechanism by which insulin resistance affects autophagy, and the study examining the trigger of autophagy by BCAAs also shows contradictory results.
This suggests that a certain limit of autophagy may have a positive effect on the regulation of lifespan, while excessive autophagy may have a negative effect, but there is no clear conclusion as to what the limit is.
Although there is no exact correlation between endogenous and exogenous BCAA levels at present, the conclusion that endogenous BCAA accumulation caused by diseases such as obesity and T2DM leads to aging and damage to the body has been very clear. Therefore, the negative effects of BCAAs on the body based on insulin resistance and various diseases can be explained.
However, elderly individuals have low concentrations of BCAAs in the plasma, but this was not the case in young individuals and children 89 , Therefore, the positive effects of BCAA supplementation on aging can also be explained.
However, theories based on endogenous BCAAs cannot explain the positive effects of insulin resistance on longevity. To date, many hypotheses have been proposed based on these contradictions. However, there are various problems, such as the lack of credible evidence and the inability to explain some of the results.
Therefore, there are no credible theories about the regulatory mechanisms of BCAAs, aging and insulin. However, two conclusions are convincing: one is that BCAAs remain an effective supplement for aging and related metabolic changes, and the other is that maintaining endogenous BCAAs within a reasonable range is indeed important for health.
Therefore, there is still a long way to go to further explore the relationship between BCAAs, longevity and insulin resistance based on existing research. Besides, the metabolites of BCAAs have been the focus of attention in recent years.
Studies were no longer limited to BCAAs study on lifespan and insulin resistance. Studying the separate amino acids of BCAAs and the metabolites of BCAAs is on the rise.
This can further research the mechanism of BCAA-regulated metabolic disorders in the body. In this review, we mainly talked about the metabolite of valine — 3-HIB. This metabolite could lead to the activation of fatty acid transportation in some organs, which is related to insulin resistance.
After that, the insulin resistance was induced in the body. In summary, the 3-HIB is a promising marker for detecting insulin resistance. However, as the essential factor of BCAAs, leucine has fewer reports about its metabolites that have an effect on insulin resistance.
So we have reason to believe that with the discovery of more metabolites of BCAAs that are in association with insulin resistance, the mechanism of BCAAs and insulin resistance will be more promising.
And these metabolites will be the potential targets to treat insulin resistance in T2DM. In conclusion, recent studies suggest that endogenous BCAAs, BCAA metabolism and mTOR-related autophagy play important roles in the relationships among BCAAs, longevity, and insulin resistance.
The recent discovery that insulin resistance may be independent of longevity has expanded our understanding of the regulatory mechanisms among the three. However, there is still no definite conclusion on the specific conditions under which BCAAs and insulin resistance extend life, shorten life, or do not change lifespan, and there is still no credible and comprehensive explanation for the different effects of BCAAs and insulin resistance on lifespan.
In addition, similar confusion occurs between BCAAs and insulin resistance. These problems are attracting increasing research interest, and the study of these problems is conducive to the elucidating the rational use of BCAAs, identifying a treatment for T2DM and the study of longevity.
YaL and YiL supervised the entire project. HY drafted the manuscript and prepared the figures. KL and JW revised the manuscript. All authors have read and agreed to the published version of the manuscript. This work was supported by grants from the CAMS Innovation Fund for Medical Sciences No.
Excess fat around the waist might also relate to chronic inflammation. This can trigger a wide range of health problems, including insulin resistance. However, body weight is just one factor that may contribute to insulin resistance. Having overweight or obesity does not mean that a person will develop insulin resistance.
A person can work with a doctor or dietitian for personalized guidance on whether diet and lifestyle changes may be beneficial. Not getting enough exercise can affect the way insulin regulates blood sugar levels. According to the American Diabetes Association , physical activity plays a vital role in keeping blood sugar levels steady.
Aim for around 30 minutes of exercise per day, at least 5 days per week. A person can also add more activity to their daily routine by taking the elevator instead of the stairs, going for a walk during their lunch break, or using a standing desk.
It is common in prediabetes, a condition that can progress to type 2 diabetes. Diet plays an essential role in preventing insulin resistance. Adding more foods that are high in fiber, protein, and heart-healthy fats to the diet can be beneficial.
Managing underlying health conditions, getting plenty of sleep, and managing stress levels can also help promote overall health and improve insulin resistance. A diagnosis of prediabetes does not mean that you will definitely advance to diabetes, though it is a high risk factor.
The good news is that prediabetes is reversible. These include reducing total carbohydrate intake; switching from processed carbs to high fiber, low GI carbs; losing weight; doing daily exercise; getting good quality sleep for 7—9 hours a night; and managing stress.
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Medical News Today. Health Conditions Health Products Discover Tools Connect. Diet tips to improve insulin resistance. Medically reviewed by Kim Rose-Francis RDN, CDCES, LD , Nutrition — By Adam Felman — Updated on March 3, Foods to eat Foods to limit Diet tips Understanding insulin resistance Causes Summary Dietary choices that support insulin sensitivity include non-starchy vegetables, whole grains, and citrus fruits.
Foods to eat. Share on Pinterest A balanced diet may help people manage their blood sugar levels. Foods to limit. Nutrition resources For more science-backed resources on nutrition, visit our dedicated hub.
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Metrics details. Nutritional weight control age increases, the risk of developing promotd 2 pgomote increases, which is associated with senile skeletal muscle dysfunction. During skeletal muscle aging, mitochondrial dysfunction, intramyocellular Inflammation and chronic pain management accumulation, increased inflammation, longeivty stress, modified activity of insulin longeviity regulatory enzymes, sensiivity reticulum stress, decreased autophagy, sarcopenia Phytochemicals and health promotion over-activated Phytochemicals and health promotion system insulun occur. These changes can impair skeletal muscle insulin sensitivity and increase the risk of insulin resistance and type 2 diabetes during skeletal muscle aging. This review of the mechanism of the increased risk of insulin resistance during skeletal muscle aging will provide a more comprehensive explanation for the increased incidence of type 2 diabetes in elderly individuals, and will also provide a more comprehensive perspective for the prevention and treatment of type 2 diabetes in elderly populations. Globally, the incidence of diabetes and the number of patients with diabetes are rising sharply, which has resulted in a worldwide public health problem that seriously threatens human health.
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