Type 2 diabetes mellitus (T2DM) is a chronic disorder that disrupts the control of blood sugar by the body. Under normal circumstances, the blood sugars are well-controlled by hormones, insulin and glucagon, released from the pancreas. Insulin lowers blood sugar by facilitating glucose uptake into cells and storage as glycogen, whereas glucagon increases blood sugar by stimulating the release of glucose into the bloodstream from the liver. Collectively, they regulate glucose homeostasis in an extremely narrow, healthy range.
In T2DM, this equilibrium is lost primarily because of insulin resistance, whereby the body cells are unable to respond to insulin effectively. While the pancreas will first oversecrete more insulin to compensate, eventually the beta cells that are committed to insulin production get damaged and cannot secrete enough insulin. This results in persistently elevated blood glucose (hyperglycemia), a feature of the disease.
Insulin resistance is a phenomenon in which muscles, fat, and liver cells cannot effectively take up glucose. As a result, glucose continues to accumulate in the blood rather than entering cells where it can be used as energy. Not only does this result in increased blood glucose, but it also stimulates the liver to generate even more glucose, piling on top of itself viciously. Excess circulating glucose damages blood vessels and nerves and is the cause of most diabetes complications.
Also, dysregulation of glucagon by pancreatic alpha cells leads to hyperglycemia in T2DM. Release of glucagon should be reduced when blood glucose levels increase after meals to avoid excess release of glucose by the liver. In type 2 diabetes, however, alpha cells secrete too much glucagon independent of high blood glucose, which exacerbates liver output of glucose and regulation of blood sugar.
Medicines are at the core of T2DM management since they enhance insulin sensitivity, activate insulin secretion, or inhibit the synthesis of glucose. For instance, medicines such as glycomet gp1 reduce blood glucose by increasing the sensitivity of the body to insulin and inhibiting hepatic release of glucose, leading to improved glucose control.
Lifestyle interventions, including diet, exercise, and weight loss, are also helpful in enhancing insulin sensitivity and glucose metabolism, frequently complementing pharmacologic therapy.
In short, type 2 diabetes mellitus disturbs blood glucose control by causing insulin resistance through induction, thus aggravating inadequate insulin and inappropriate glucagon secretion. This leads to reduced glucose uptake and elevated glucose generation, ultimately resulting in chronic hyperglycemia. The knowledge of these mechanisms becomes the key to successful treatment with medications such as glycomet GP1 and strict lifestyle changes.
Disclaimer: This is a medical information article only and not meant to be a substitute for professional medical advice. Use a healthcare practitioner for individualised diagnosis and treatment of diabetes.
