Journal of Diabetology

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Perspective - Journal of Diabetology (2022) Volume 6, Issue 3

Diabetes mellitus and its adverse effects under obese conditions.

Amelia Saunders*

Department of Endocrinology and Metabolism Research Center (EMRC), Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

*Corresponding Author:
Amelia Saunders
Department of Endocrinology and Metabolism Research Center (EMRC)
Vali-Asr Hospital, School of Medicine
Tehran University of Medical Sciences, Tehran,

Received: 13-May-2022, Manuscript No. AADY-22-63779; Editor assigned: 16-May-2022, PreQC No. AADY-22-63779(PQ); Reviewed: 24-May-2022, QC No. AADY-22-63779; Revised: 27-May-2022, Manuscript No. AADY-22-63779(R); Published: 30-May-2022, DOI:10.35841/aady-6.3.114

Citation: Saunders A. Diabetes mellitus and its adverse effects under obese conditions. J Diabetol. 2022;6(3):114

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Diabetes Mellitus (DM) is a chronic disease that affects the metabolism of carbohydrates, proteins, and fats. It is caused by a lack of insulin secretion as a result of the beta-langerhans islet cells of the pancreas' gradual or significant failure to make insulin, or by deficiencies in insulin uptake in peripheral tissue. Type 1 diabetes and type 2 diabetes are the two most common types of diabetes. Autoimmunity is thought to play a crucial element in the pathogenesis of type 1 diabetes. Other autoimmune illnesses, such as Graves' disease, Hashimoto's thyroiditis, and Addison's disease, have a strong link to type 1 diabetes. The prevalence of type 1 diabetes rises when these conditions are present [1].

Beta-cell dysfunction is a major element in the transition from prediabetes to diabetes. Following the transition from normal to impaired glucose tolerance, postprandial blood glucose levels rise at first. As the inhibition of hepatic gluconeogenesis fails, fasting hyperglycemia may develop. Despite the fact that the pathogenesis of type 1 and type 2 diabetes differs, the majority of the sequelae are the same, including macrovascular and microvascular problems. Microvascular and metabolic problems appear to be linked to abnormal glycemia [2].


An excess accumulation of adipose tissue to the point where it compromises both physical and psychosocial health and well-being is classified as obesity. Obesity is a public health emergency in both developed and underdeveloped countries. In several countries around the world, the frequency is rapidly increasing. If the disease's economic expenses, social dangers, morbidity, and death are considered, the pandemic must be prevented [3].

Obesity and type 1 diabetes

The obesity epidemic is linked to the increased incidence of type 2 diabetes in children and adults. A similar aetiology is also to blame for the rise in type 1 diabetes cases. While the underlying pathophysiology of type 1 diabetes, which is autoimmune in nature, is still being researched, the specific mechanism causing the rise in the incidence of type 1 diabetes, particularly in young age groups, remains unknown.

According to twin studies, environmental and genetic variables both contribute to the genesis of type 1 diabetes. Furthermore, a considerable increase in type 1 diabetes incidence in immigrants from lower to higher incidence locations indicates the role of environmental variables in the aetiology of diabetes. Short-term or no nursing, exposure to cow's milk protein, and infection with enterovirus or rubella have all been explored as possible causes of type 1 diabetes. None of these triggering factors, however, has been proven to be the sole reason.

Obesity and type 2 diabetes

Obesity has become more prevalent in recent years, drawing attention to the problem's global relevance. Approximately two-thirds of the adult population in the United States is considered overweight or obese. Similar patterns can be seen all around the world. Obesity has been related to a variety of medical, psychological, and social issues, the most serious of which is type 2 diabetes.

Insulin resistance is linked to both type 2 diabetes and obesity. Despite being insulin resistant, most fat people do not suffer hyperglycemia. Under normal circumstances, pancreatic Betacells of the islet of Langerhans release sufficient amounts of insulin to counteract insulin level deficits, resulting in normal glucose tolerance

Endothelial dysfunction is associated with obesity/insulin resistance in diabetes and prediabetes (those with impaired glucose tolerance and/or impaired fasting glucose) throughout the natural history of type 2 diabetes. Beta-cells should not be able to fully adjust for decreased insulin sensitivity in order to develop insulin resistance and obesity, resulting in type 2 diabetes. Because of the non-esterified fatty acids (NEFAs) released by adipose tissue in obese patients, it's possible that insulin resistance and Beta-cell dysfunction are connected [4].

Obesity and insulin resistance

Insulin sensitivity changes during the course of a person's life. Insulin resistance can be seen during puberty, pregnancy, and the ageing process, for example. Furthermore, lifestyle changes such as increased carbohydrate intake and greater physical exercise are linked to changes in insulin sensitivity. The most important determinant in the development of metabolic disorders is obesity. By secreting hormones, glycerol, and other compounds such as leptin, cytokines, adiponectin, and proinflammatory substances, as well as producing NEFAs, adipose tissue influences metabolism. The secretion of these chemicals is higher in fat people.

Another important element that influences insulin sensitivity is body fat distribution. Insulin resistance is linked to BMI regardless of the degree of weight gain. Because of variances in body fat distribution, insulin sensitivity varies greatly among lean people. Individuals with a more peripheral fat distribution had higher insulin sensitivity than those with a more central fat distribution (ie, in the abdomen and chest area).

Differences in adipose tissue distribution help explain how subcutaneous and intra-abdominal fat have different metabolic consequences. Intra-abdominal fat is more closely linked to the genes that produce proteins as well as the specific types of proteins involved in energy production. The amount of adiponectin released by omental adipocytes is greater than that secreted by subcutaneous adipocytes. Furthermore, the amount released by these omental adipocytes is inversely related to body weight gain.

Obesity and β-cell dysfunction

Despite their vulnerability, Beta-cells play an important function in insulin regulation. The amount of insulin released by Beta-cells varies and changes depending on the stimulus's quantity, nature, and mode of administration. As a result, Beta-cells serve a critical role in ensuring that blood glucose concentrations in healthy people stay within a somewhat typical physiological range. Insulin sensitivity and regulation of Beta-cell function both diminish with fat.

Insulin-resistant people, thin or overweight, have higher insulin responses and lower hepatic insulin clearance than insulinsensitive people. A continual feedback link exists between Beta-cells and insulin-sensitive tissues in a normal healthy patient. If the adipose tissue, liver, and muscles require more glucose, the Beta-cells will produce more insulin. Changes in insulin sensitivity must be matched by a relatively opposite shift in circulating insulin levels if glucose levels to remain stable.

Failure to carry out this procedure results in a dysregulation of glucose levels and the onset of diabetes. If the Beta cells are healthy, there is an adaptive response to insulin resistance that allows normal glucose levels to be maintained. When pancreatic Beta-cells are damaged, altered glucose tolerance or fasting glucose might occur, which can lead to type 2 diabetes [5].


Diabetes and obesity are chronic diseases that are becoming more common around the world. Diabetes and insulin resistance have a substantial association with BMI. NEFA, glycerol, hormones, cytokines, pro inflammatory chemicals, and other compounds implicated in the development of insulin resistance are all increased in obese people. Diabetes is caused by insulin resistance combined with impaired Beta-cell activity. Early weight gain has been linked to the development of type 1 diabetes. The development of insulin resistance and the impairment of Beta-cell function are both linked to NEFA. Based on these findings, new techniques to managing and preventing diabetes in obese people must be examined and investigated.


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