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Related Concept Videos

Oral Hypoglycemic Agents: Glinides01:06

Oral Hypoglycemic Agents: Glinides

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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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Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

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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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Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

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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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Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

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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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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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Diabetes Mellitus: Overview and Type I Subtype01:22

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Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels due to inadequate insulin production, insulin resistance, or both. The condition affects millions worldwide and can significantly impact their health and quality of life.
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Diabetes, bone and glucose-lowering agents: basic biology.

Beata Lecka-Czernik1,2,3

  • 1Departments of Orthopaedic Surgery, MS 1008, Health Sciences Campus, The University of Toledo, 3000 Arlington Avenue, Toledo, OH, 43614, USA. beata.leckaczernik@utoledo.edu.

Diabetologia
|April 24, 2017
PubMed
Summary

Diabetes compromises bone quality, leading to skeletal fragility. This review explores how diabetes affects bone through metabolic and vascular pathways, impacting bone healing and treatment strategies.

Keywords:
AGEsBone qualityBone remodellingBone vasculatureGlucoseGlucose-lowering therapiesMuscleOsteoblastOsteoclastReviewStem cells

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Area of Science:

  • Endocrinology
  • Metabolic Bone Disease
  • Diabetology

Background:

  • Diabetes mellitus is associated with increased skeletal fragility, independent of bone mass or trauma.
  • Bone remodeling and turnover are impaired in both type 1 and type 2 diabetes, affecting bone material quality.
  • Existing research often overlooks the specific impact of diabetes on bone health.

Purpose of the Study:

  • To review basic science evidence on how diabetes affects bone.
  • To discuss the cellular and molecular mechanisms underlying diabetes-induced bone defects.
  • To outline the safety of glucose-lowering agents and potential therapeutic strategies for diabetes-related bone syndrome.

Main Methods:

  • Literature review of basic science evidence.
  • Analysis of cellular and molecular mechanisms.
  • Discussion of clinical and therapeutic implications.

Main Results:

  • Diabetes impairs bone metabolism through altered glucose metabolism, advanced glycation end-products (AGEs), and compromised microvascular and muscle endocrine function.
  • Diabetes negatively impacts the bone stem cell niche and fracture healing.
  • Current glucose-lowering therapies have varying safety profiles regarding bone health.

Conclusions:

  • Diabetes significantly impacts bone quality and integrity through multiple pathways.
  • Understanding these mechanisms is crucial for developing targeted therapies.
  • Future research should focus on treatments that address both glycemic control and bone health.