Diabetes Case Reports

Pathophysiology of Diabetes Mellitus and its Complications

Henry Paul^* Department of Medicine, New York University School of Medicine, New York, USA
^*Correspondence: Henry Paul, Department of Medicine, New York University School of Medicine, New York, USA, Email:

Received: 15-Apr-2022, Manuscript No. 2572-5629-22-16849; Editor assigned: 20-Apr-2022, Pre QC No. 2572-5629-22-16849 (PQ); Reviewed: 28-Apr-2022, QC No. 2572-5629-22-16849; Revised: 10-May-2022, Manuscript No. 2572-5629-22-16849 (R); Published: 17-May-2022

About the Study

The pathophysiology of diabetes is interrelated to insulin levels in the body as well as the body's ability to use insulin. In type 1 diabetes, no insulin is secreted at all, but in type 2 diabetes, the peripheral tissues oppose insulin's actions. Insulin is generally produced by pancreatic beta cells in response to increased blood glucose levels. Glucose is required by the brain in order for normal processes to continue. Diabetes Mellitus (DM) is a category of metabolic illnesses distinguished by hyperglycemia. Chronic hyperglycemia is linked to protracted deterioration, and impairment, including eventual organ failure in a variety of organs, including the eyes, kidneys, nerves, heart, and blood vessels. Type 2 Diabetes Mellitus (T2DM) is caused by a number of reasons, the most important of which are insufficient insulin secretion (insulin deficit) and/or decreased tissue responses to insulin (insulin resistance) at one or more locations along the complicated hormone action pathways. Insulin resistance and deficiency typically coexist, albeit the contribution to hyperglycemia varies greatly across the T2DM spectrum.

Genetic and environmental factors

Hyperinsulinemia, which is defined as the inability of insulin to lower plasma glucose levels by suppressing hepatic glucose production and stimulating glucose utilization in skeletal muscle and adipose tissue, is often exacerbated by impaired insulin secretion. In the presence of physiologically possible levels of insulin in humans, glucose uptake is decreased in subjects with T2DM compared to normal subjects, confirming that glucose uptake is differentiated. Inefficient glucose utilization is gradually replaced by the cellular metabolism of fats and proteins for energy as a result of insulin resistance. Genetic and environmental factors can have a role in insulin resistance. Insulin resistance can be caused by a family history, but it can also be caused by many environmental factors such as obesity, comorbidities, and central adiposity (visceral fat). The exact aetiology of insulin resistance in any one patient is unknown, although it could include problems with insulin-mediated cell signaling pathways, decreased insulin-stimulated muscle glycogen synthesis, or even a lack of insulin receptors (particularly in skeletal muscle, liver, and adipose tissue in obese subjects).

Due to the variability of T2DM, the proportional contributions of insulin secretion and insulin resistance to the development of hyperglycemia might fluctuate. Insulin resistance is, in most cases, the first evident problem in people who have prediabetes. Enhanced insulin secretion may initially compensate for insulin resistance; however, early phase insulin secretion is hindered. Insulin sensitivity deteriorates by around 40 percentage points in the shift from normal glucose tolerance to impaired glucose tolerance and DM, while insulin secretion deteriorates 3to5 fold. Chronic hyperglycemia in people with diabetes can lead to a worsening of insulin sensitivity and secretion (glucotoxicity), which is exacerbated by high levels of free fatty acids (lipotoxicity). Increased hepatic glucose output and adipocyte dysfunction are two more increasingly well-understood processes that contribute to the pathophysiology of T2DM. Insulin is generally produced into the portal vein after glucose administration, where it is taken up by the liver and decreases hepatic glucose production. The two sources of glucose input (from the liver and the gastrointestinal tract) will result in significant hyperglycemia if the liver does not recognize the insulin signal and continues to manufacture glucose. Increased hepatic glucose production in T2DM is hypothesized to be linked to insulin resistance and is closely linked to the severity of fasting hyperglycemia.

Deranged metabolism and altered fat disposal are implicated in the aetiology of glucose intolerance in T2DM, according to a growing body of research. Because fat cells resist insulin's antilipolytic impact, chronically increased plasma free fatty acid levels drive gluconeogenesis, create hepatic/muscle insulin resistance, and impede insulin secretion in those who are predisposed. Lipotoxicity is the term for the disruptions caused by free fatty acids. Aside from this, defective fat cells create an excess of insulin resistance-inducing, inflammatory, and atherosclerotic-provoking cytokines and fail to secrete enough levels of insulin-sensitizing adipocytokines (adiponectin). Furthermore, the pattern of fat disposition in T2DM is abnormal, owing to the fact that enlarged adipocytes (in visceral fat) are insulin-resistant and have a reduced capacity to store fat, resulting in lipid overflow into muscle, liver, and possibly β-cell, exacerbating muscle/hepatic insulin resistance and impairing insulin secretion. Adipocytokines, which are proinflammatory cytokines, are abundant in individuals. The increased free fatty acids in the liver cells are converted to triglycerides, which build up and produce steatosis (or fatty liver), which can lead to Nonalcoholic Steatohepatitis (NASH) and ultimately cirrhosis.

Conclusion

The fact that many people with T2DM are obese makes these changes in adipocyte function all the more important. Multiple systems, including muscle, liver, β-cell, and fat cell, are involved in the development of glucose intolerance in T2DM (accelerated). Β-cell, fat cell (increased glucose reabsorption), gastrointestinal tract (incretin deficiency/resistance), cell (hyperglucagonemia), kidney (increased glucose reabsorption), and brain (insulin resistance). These eight players make up the ominous octet, which necessitates the use of combination therapy. Treatment should focus on rectifying identified pathophysiological problems rather than simply lowering. Early treatment may assist to prevent or decrease the progression of β- cell failure.