A Concise Clinicopathological Handbook of Diabetes Mellitis


Diabetes mellitus (DM) is one of the most common chronic illnesses worldwide. According to the World Health Organization, about By 2025, Asian developing countries would account for 60% of diabetic patients. Insulin, as well as other hormones, are produced by pancreatic beta cells. Increased blood sugar levels are required for insulin release above basal levels, and insulin, as an anabolic hormone, will aid in the process of glycogenesis, protein synthesis, and glucose uptake in muscles and adipose tissue. Type I Diabetes Mellitus is caused by a complex interaction of inherited, environmental, and immunological variables that lead to immune system dysfunction, pancreatic cell damage, and insulin deficiency. There is strong evidence of lymphocytic insulinitis and cell-mediated autoimmunity, with helper/inducer and cytotoxic/suppressor T lymphocyte subsets, as well as natural killer cells, present. Because of compensatory over-secretion of insulin by pancreatic islets, glucose tolerance remains normal in the early stages despite insulin resistance. The pathophysiology of long-term diabetic consequences such microvascular disease (microangiopathy), retinal disease (retinopathy), kidney disease (nephropathy), and nerve dysfunction (neuropathy) is currently being studied extensively. Pioglitazone and rosiglitazone are rapidly absorbed and mainly bound by serum albumin after oral dosing. Both of these medicines go through CYP450 metabolism, which is mediated by several isozymes. Increased frequency of infections, sepsis, preeclampsia, postpartum haemorrhage, foetal malformations, large newborns, labour irregularities, and unexpected foetal deaths are all maternal problems related with diabetes during pregnancy.

Author(s) Details

Sourya Acharya
Department of Internal Medicine, Datta Meghe Institute of Medical Sciences (Deemed to be University), Jawaharlal Nehru Medical College Sawangi (Meghe), Wardha, Maharashtra, India.

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