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Localization, Identification, and Excision of Murine Adipose Depots
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[Kidney, adipose tissue, adipocytes--what's new?]

Max Lafontan1

  • 1Équipe 1, unité Inserm 1048, institut des maladies cardiovasculaires et métaboliques, BP 84225, 31432 Toulouse cedex 4, France. max.lafontan@inserm.fr

Nephrologie & Therapeutique
|December 16, 2010
PubMed

Insights

Obesity may directly cause kidney disease through adipose tissue. This review explores how fat cell metabolism and endocrine functions contribute to obesity-related kidney damage and lipotoxicity.

Area of Science:

  • Nephrology
  • Endocrinology
  • Metabolic Syndrome

Background:

  • Obesity is increasingly linked to kidney diseases like obesity-related glomerulopathy.
  • The role of adipose tissue's endocrine functions in kidney disease initiation and progression is under investigation.

Purpose of the Study:

  • To review recent advances in adipose tissue physiology and fat cell metabolism.
  • To explore the potential contribution of adipose tissue dysfunction to kidney lipotoxicity and chronic kidney diseases in obesity.

Main Methods:

  • Literature review of recent advances in adipose tissue metabolism and physiology.
  • Analysis of adipose tissue endocrine functions, including hormone secretion and immune cell infiltration.

Main Results:

  • Adipose tissue functions as an endocrine organ, secreting hormones like leptin, adiponectin, and apelin.
  • Expanding adipose tissue in obesity is infiltrated by immune cells, and its secretory functions may be altered.

Conclusions:

  • Dysregulation of lipid storage, fatty acid release, and hormone secretion by adipose tissue may contribute to kidney lipotoxicity.
  • Adipose tissue dysfunction is a potential driver of obesity-related kidney diseases.

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