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The biological clock is involved in many aspects of regulating complex physiology in all animals. It was in 1935 when German zoologists, Hans Kalmus and Erwin Bünning, discovered the existence of circadian rhythm in Drosophila melanogaster. However, the internal molecular mechanisms behind the circadian clock remained a mystery until 1984, when Jeffrey C. Hall, Michael Rosbash, and Michael W. Young discovered the expression of the Per gene oscillating over a 24-hour cycle. In subsequent...
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Parallel Measurement of Circadian Clock Gene Expression and Hormone Secretion in Human Primary Cell Cultures
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The molecular clock mediates leptin-regulated bone formation.

Loning Fu1, Millan S Patel, Allan Bradley

  • 1Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030; Bone Disease Program of Texas, Baylor College of Medicine, Houston, Texas 77030, USA.

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Summary

Leptin and the molecular clock regulate bone formation. Clock genes mediate sympathetic signaling

Keywords:
Non-programmatic

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Area of Science:

  • Endocrinology
  • Chronobiology
  • Bone Biology

Background:

  • Leptin is a key regulator of bone remodeling and mass.
  • Circadian clock genes (Per and Cry) influence bone mass, with deficiencies leading to high bone mass.
  • Per-deficient mice show increased bone mass after leptin infusion, suggesting a role for clock genes in leptin-mediated bone regulation.

Purpose of the Study:

  • To investigate the role of molecular clock genes in mediating sympathetic nervous system regulation of bone formation by leptin.
  • To elucidate the mechanisms by which leptin, via sympathetic signaling and clock genes, influences osteoblast proliferation and bone mass.

Main Methods:

  • Analysis of clock gene expression in osteoblasts under sympathetic nervous system and leptin influence.
  • Assessment of the impact of clock genes on G1 cyclin expression and osteoblast proliferation.
  • Evaluation of leptin's effect on AP-1 gene expression and its role in cyclin D1 upregulation.

Main Results:

  • Sympathetic nervous system and leptin regulate clock gene expression in osteoblasts.
  • Clock genes inhibit osteoblast proliferation by suppressing G1 cyclin expression.
  • Leptin counteracts this inhibition by upregulating AP-1, promoting cyclin D1 expression, osteoblast proliferation, and bone formation.

Conclusions:

  • Leptin modulates osteoblast proliferation and bone formation through dual, antagonistic pathways involving sympathetic signaling and the molecular clock.
  • The molecular clock plays a critical role in mediating the sympathetic regulation of bone remodeling.
  • Understanding these pathways offers insights into maintaining bone homeostasis and potential therapeutic targets.