Related Experiment Videos

Antihyperglycaemic and antiperoxidative roles of acarbose in type 2 diabetes mellitus are possibly mediated through

Jatwa Rameshwar1, Kar Anand

  • 1School of Life Sciences, DA University, Indore, India.

Clinical and Experimental Pharmacology & Physiology
|October 18, 2006
PubMed

Insights

Acarbose treatment for type 2 diabetes in mice normalized thyroid hormone levels and reversed hyperglycemia. These findings suggest thyroid hormones play a role in acarbose

Area of Science:

  • Endocrinology
  • Pharmacology
  • Biochemistry

Background:

  • Type 2 diabetes mellitus is characterized by hyperglycemia and oxidative stress.
  • Acarbose is an established antihyperglycemic agent.
  • The role of thyroid hormones in acarbose's mechanism of action is not fully understood.

Purpose of the Study:

  • To investigate the involvement of thyroid hormones in the antihyperglycemic and antiperoxidative effects of acarbose.
  • To examine the impact of acarbose on thyroid hormone levels in a mouse model of type 2 diabetes.

Main Methods:

  • Dexamethasone-induced type 2 diabetes in mice was used.
  • Serum concentrations of thyroid hormones, insulin, and glucose were measured.
  • Lipid peroxidation (LPO), reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activity were assessed in renal and cardiac tissues.

Main Results:

  • Dexamethasone administration induced hyperglycemia, increased insulin and LPO, but decreased thyroid hormones and antioxidant enzyme activity (SOD, CAT).
  • Acarbose treatment reversed these abnormalities, increasing thyroid hormone levels and restoring biochemical parameters.
  • Acarbose normalized serum insulin and glucose, reduced tissue LPO, and modulated antioxidant enzyme activity and GSH content.

Conclusions:

  • Thyroid hormones are likely involved in the antihyperglycemic and antiperoxidative effects of acarbose.
  • Acarbose may exert its therapeutic benefits in type 2 diabetes partly through modulation of thyroid hormone levels.
  • These findings provide novel insights into the mechanism of action of acarbose in managing type 2 diabetes.

Related Concept Videos

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
Acarbose and miglitol are typically...
Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood glucose levels...
Diabetes Mellitus: Type 2 and Gestational01:22

Diabetes Mellitus: Type 2 and Gestational

Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Oral Hypoglycemic Agents: Sulfonylureas01:17

Oral Hypoglycemic Agents: Sulfonylureas

Sulfonylureas are oral hypoglycemic agents utilized in treating type 2 diabetes. They are characterized by their unique sulfonylurea chemical structure. The family of sulfonylureas is divided into generations. First-generation sulfonylureas, including tolbutamide (Orinase), chlorpropamide (Diabinese), and tolazamide (Tolinase), trigger insulin release from pancreatic β cells and enhance peripheral tissues' insulin sensitivity. The second-generation members, such as glipizide (Glucotrol),...