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Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
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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...
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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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Oral Hypoglycemic Agents: Glinides01:06

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Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively...
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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.
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Hypoglycemia and Glucagon01:15

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Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
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Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test OGTT and Insulin Tolerance Test ITT
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Trimethylamine N-oxide impairs β-cell function and glucose tolerance.

Lijuan Kong1,2,3, Qijin Zhao1,2,3, Xiaojing Jiang1,2,3

  • 1State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

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|March 22, 2024
PubMed
Summary
This summary is machine-generated.

Trimethylamine N-oxide (TMAO) impairs glucose-stimulated insulin secretion and beta-cell function, contributing to type 2 diabetes. Inhibiting TMAO production may offer a new therapeutic strategy for managing diabetes.

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Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Molecular Biology

Background:

  • Beta-cell dysfunction and loss are key features of type 2 diabetes (T2D).
  • Elevated levels of trimethylamine N-oxide (TMAO) are observed in diabetic patients.
  • The direct impact of TMAO on beta-cell function requires further elucidation.

Purpose of the Study:

  • To investigate the direct effects of TMAO on beta-cell function and viability.
  • To explore the mechanisms by which TMAO influences beta-cell function.
  • To assess the therapeutic potential of inhibiting TMAO production in T2D.

Main Methods:

  • In vitro studies using MIN6 cells and primary human/mouse islets.
  • In vivo studies in male C57BL/6J mice, db/db mice, and choline diet-fed mice.
  • Assessment of glucose-stimulated insulin secretion (GSIS), beta-cell proportion, glucose tolerance, calcium transients, ER stress, and apoptosis.

Main Results:

  • TMAO significantly decreased GSIS and impaired beta-cell function in vitro and in vivo.
  • TMAO inhibited calcium transients via NLRP3 inflammasome-related cytokines and induced Serca2 loss.
  • TMAO promoted beta-cell ER stress, dedifferentiation, apoptosis, and inhibited transcriptional identity.
  • Inhibition of TMAO production ameliorated beta-cell dysfunction and improved glucose tolerance.

Conclusions:

  • TMAO directly impairs beta-cell function and survival, contributing to T2D pathogenesis.
  • TMAO exerts its detrimental effects through mechanisms involving calcium signaling, Serca2, and ER stress.
  • Inhibiting TMAO production represents a promising therapeutic avenue for T2D treatment.