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Diabetes and Obesity Research


Diabetes and Obesity Overview

Obesity and diabetes and related diseases have gradually become one of the research hotspots. Since the 1980s, the prevalence of obesity and diabetes has gradually increased. Obesity is induced by many complicated situations, and it frequently induces diabetes, dyslipidemia, atherosclerosis, hypertension, etc., which is an independent risk factor for diabetes and cardiovascular disease.

Relationship of Diabetes and Obesity

Diabetes and Obesity Research

Obesity refers to excessive accumulation and distribution of fat in the body, which is the result of a combination of genetic and environmental factors. Clinically, the body mass index (BMI) is commonly used to measure the level of obesity. In addition, the waist circumference, body-specific gravity, body fat distribution, energy intake, and energy consumption can be used as diagnostic parameters of obesity. The criteria published by the WHO in 1997 are: BMI as the diagnostic criteria for obesity: BMI < 18.5 for low body weight, 18.5 < BMI < 24.9 for normal, 25 < BMI < 30 for overweight, BMI > 30 for obesity, 35 to 39.9 is II degree (severe), and ≥ 40 is III degree (very severe). Waist circumference: Male 94cm, female 80 cm is considered obese. In recent years, 90% of patients with type 2 diabetes have obesity. Many lateral surveys have confirmed that the incidence of obesity is associated with the incidence of diabetes in the same population. The incidence of diabetes in the overweight is 2.9 times of the normal weight. Prospective studies have also confirmed that weight gain is also an important risk factor for diabetes. A follow-up study of 11428 women aged 30-55 years has been reported, indicating that women with a BMI between 23 and 25 are at 4 times more likely to develop type 2 diabetes than women with a BMI less than 22. In summary, weight gain is associated with an increased risk of developing type 2 diabetes. Although the pathogenesis of diabetes is still not fully understood, it is certainly related to genetic and environmental factors. Among environmental factors, the most important is obesity.

Diabetes and Obesity Research Status

The pathophysiological mechanism by which obesity develops into diabetes is not fully understood. It has been confirmed that due to the accumulation of body fat, insulin resistance, hyperinsulinemia, utilization of glucose by muscles and other tissues are reduced, and then glucose tolerance is reduced, and eventually develops into diabetes. In addition, the uptake of free fatty acids (FFA) and the increase of oxidation are one of the important reasons for the development of obesity into diabetes. A series of studies have shown that elevated levels of FFA in plasma increase the rise in hepatic glycogen and reduce the ability of the liver to clear insulin, resulting in hyperinsulinemia. High levels of FFA inhibit the utilization of insulin-stimulated sugars in skeletal muscle and the synthesis of muscle glycogen. In addition, studies have shown that FFA can promote B cells to secrete insulin and stimulate liver synthesis of VLDL (very low-density lipoprotein) under certain conditions. Therefore, in obese patients, the oxidation of FFA increases is accompanied by a decrease in sugar oxidation and sugar storage, which results in islet-mediated inhibition of hepatic gluconeogenesis. The sensitivity of the liver and skeletal muscle to insulin decreases, insulin inactivation decreases and secretion increases, eventually leading to insulin resistance and hyperinsulinemia. When obese patients' beta cells can compensate for insulin resistance, they can maintain normal blood sugar. In order to reimburse hyperglycemia, the level of insulin is increasing, eventually leading to islet beta cell failure, and development of diabetes. Studies have shown that visceral obesity is more likely to cause insulin resistance than peripheral fat because FFA directly enters the portal vein. Recent studies have found that tumor necrosis factor alpha (TNF-α) plays an important role in insulin resistance in obese patients. It has been found that the expression of TNF-α is significantly increased in adipose tissue of obese patients with insulin resistance and obese type 2 diabetes patients. The mechanism by which TNF-α aggravates insulin resistance includes several aspects: accelerating lipolysis and leading to elevated FFA levels; TNF-α produced by fat cells of obese people inhibits the activity of tyrosinase in muscle tissue insulin receptors by endocrine and paracrine actions to reduce the action of insulin. TNF-α has a down-regulation effect on glucose transporter-4 (GLUT4) in adipocytes. Other factors, such as leptin, are associated with obesity and insulin resistance and may be involved in the development of obesity to diabetes. Early life also affects the development of obesity and diabetes. The body weight at birth and in the first year after birth is also associated with obesity, diabetes, hypertension, and hyperlipidemia in late adulthood. Low birth weight is associated with abdominal obesity that has occurred in recent years. Early malnutrition limits fat cell development and visceral fat is more likely to accumulate fat in adulthood than in other parts of the body to store energy. Early malnutrition also affects the growth and development of islet cells, making islet cells more prone to failure and prone to diabetes. Therefore, proper weight loss is beneficial to prevent obese patients from developing into diabetes. For patients with existing diabetes, although the weight loss cannot completely restore the damaged islet function, it can significantly improve the control of diabetes and reduce the dose of hypoglycemic drugs. Some reports now suggest that proper weight loss can reduce the mortality rate of diabetes. Many studies have confirmed that reducing body weight can prevent or delay the development of obesity to diabetes. Studies have shown that women lose more than 5 kg in 10 years and the risk of developing diabetes can be reduced by 50%. In one study, the patients with abnormal glucose tolerance (IGT) were randomly divided into two groups, one group to reduce weight and increase exercise; the other group was the control group, and after 5 weeks, the weight of the treatment group decreased by 2.0-3.3 kg, while the control group increased by 0.2 to 2.0 kg, the incidence of diabetes in the treatment group was 11%, and the control group is 29%. Studies have shown that weight loss can improve glycemic control in diabetes, and some patients may not even return blood sugar conditions to normal conditions without drug interference; The patient loses weight is positive related with the blood sugar control. Weight loss not only increases the sensitivity of surrounding tissues to insulin but also increases the ability of insulin to inhibit hepatic glucose output. In patients with increased sugar secretion and delayed secretion in the sugar load test, insulin secretion can return to normal after weight loss. After losing weight, plasma FFA decreases fat oxidation, and glucose storage and utilization increase. Weight loss increases the use of sugar by fat and muscle tissue and increases the binding rate of insulin and insulin receptors, which helps glucose to move to the muscles. And it also increases the activity of tyrosine kinases in adipocytes, thereby increasing the role of insulin in adipocytes. Obesity and diabetes patients can help to improve various lipid metabolism disorders after losing weight. For example, studies have shown that the weight loss of diabetic patients is 6.9 kg or more, and HDL-C (high-density lipoprotein) cholesterol is significantly increased. The more weight loss, the more obvious the improvement of lipid metabolism disorder. The American Diabetes Association recommends weight loss as the first line of treatment for diabetic lipid metabolism disorders and the primary preventive measure for cardiovascular disorders associated with diabetic lipid metabolism disorders. Epidemiological investigations have shown that the development of diabetes complications is highly correlated with glycemic control. Strict control of blood sugar can reduce the incidence of diabetic retinopathy by 70%. Obese diabetic patients, with weight loss, help blood sugar to be well controlled and delay the onset of diabetes complications. A population-based study suggests that insulin resistance can be reduced after weight loss, thereby reducing the risk of cardiovascular disease in the clinical phase of diabetes. Therefore, weight loss is beneficial to prevent the occurrence of diabetic complications.

References:

  1. Leong K S, Wilding J P. Obesity and diabetes. Bailliere’s Best Pact Res Clin Endocrinol Metab. 1999, 13(2):221-237.
  2. Polsky S, Ellis S L. Obesity, insulin resistance, and type 1 diabetes mellitus. Curr Opin Endocrinol Diabetes Obes. 2015, 22(4):277.
  3. Cătoi A F, Pârvu A, Mureşan A, et al. Metabolic Mechanisms in Obesity and Type 2 Diabetes: Insights from Bariatric/Metabolic Surgery. Obesity Facts. 2015, 8(6):350-363.
  4. Temelkova-Kurktschiev T, Stefanov T. Lifestyle and genetics in obesity and type 2 diabetes. Experimental & Clinical Endocrinology & Diabetes. 2011, 120(01):1-6.

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