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Hormones Regulating Blood Glucose01:16

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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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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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Hyperglycemia impairs osteoblast cell migration and chemotaxis due to a decrease in mitochondrial biogenesis.

Heena Pahwa1, Md Touseef Khan1, Kunal Sharan2,3

  • 1Department of Molecular Nutrition, CSIR-Central Food Technological Research Institute, Mysuru, 570020, India.

Molecular and Cellular Biochemistry
|April 19, 2020
PubMed
Summary
This summary is machine-generated.

High glucose levels in diabetes impair osteoblast cell migration and chemotaxis, potentially explaining increased bone fragility despite normal bone mineral density.

Keywords:
ChemotaxisDiabetesMigrationMitochondrial biogenesisOsteoblastSkeletal fragility

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Endocrinology

Background:

  • Diabetes mellitus is linked to increased skeletal fragility and fracture risk.
  • Mechanisms underlying diabetes-associated bone fragility are not fully understood.
  • Previous osteoblast studies yielded ambiguous results due to supraphysiological glucose concentrations.

Purpose of the Study:

  • To investigate the effects of physiologically relevant high glucose levels (11.1 mM) on MC3T3-E1 osteoblast cell functions.
  • To elucidate the impact of hyperglycemia on osteoblast differentiation, proliferation, migration, and mitochondrial dynamics.

Main Methods:

  • Cultured MC3T3-E1 osteoblast cells exposed to 11.1 mM high glucose.
  • Assessed cell proliferation, differentiation, mineralization, migration, and chemotaxis.
  • Analyzed associated cell signaling, Dynamin 2 localization, and mitochondrial dynamics (DRP1 expression).

Main Results:

  • High glucose increased osteoblast differentiation and mineralization but did not affect proliferation.
  • Osteoblast migration and chemotaxis were significantly reduced under high glucose conditions.
  • Aberrant Dynamin 2 localization and a shift towards fused mitochondria (decreased DRP1) were observed.

Conclusions:

  • Hyperglycemia reduces osteoblast cell migration and chemotaxis.
  • This impaired migration may lead to inefficient osteoblast movement, uneven mineralization, and skeletal fragility in type 2 diabetes patients.
  • Findings suggest a novel mechanism for bone fragility in diabetes independent of bone mineral density.