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Updated: May 16, 2025

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
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From fat to filter: the effect of adipose tissue-derived signals on kidney function

Nermin Ahmed1, Carolina Dalmasso2, Meghan B Turner1

  • 1Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY, USA.

Nature Reviews. Nephrology
|April 2, 2025
PubMed

Insights

Obesity severely impacts kidney health through mechanisms like inflammation and altered nerve activity, increasing risks for chronic kidney disease and failure. Understanding this adipose tissue-kidney crosstalk is crucial for preventing renal decline.

Area of Science:

  • Nephrology
  • Endocrinology
  • Physiology

Background:

  • Obesity presents significant risks for renal health, leading to chronic kidney disease, kidney failure, and mortality.
  • Multiple direct and indirect pathways link obesity to kidney damage, including hormonal imbalances, inflammation, and altered hemodynamics.

Purpose of the Study:

  • To elucidate the complex mechanisms through which obesity affects kidney function.
  • To explore the role of the adipose tissue-brain-kidney axis in obesity-related renal decline.

Main Methods:

  • Review of physiological and pathophysiological mechanisms connecting adipose tissue expansion to renal dysfunction.
  • Analysis of the impact of adipokines, inflammation, insulin resistance, and lipotoxicity on kidney health.
  • Examination of the bidirectional communication between adipose tissue, the brain, and the kidneys.

Main Results:

  • Obesity-induced adipose tissue expansion triggers hemodynamic changes, inflammation, fibrosis, and increased filtration barrier permeability.
  • Adipose tissue dysfunction, exacerbated by insulin resistance and lipotoxicity, contributes to a pro-inflammatory and pro-fibrotic renal environment.
  • The adipose tissue-brain-kidney axis plays a key role, with sympathetic nerve activity modulated by adipose tissue signaling.

Conclusions:

  • Obesity-associated renal decline is driven by a complex interplay of metabolic, inflammatory, and neural factors.
  • Bidirectional crosstalk between adipose tissue and kidneys is fundamental to understanding and potentially treating obesity-related kidney disease.
  • Targeting these interconnected mechanisms may offer new therapeutic strategies for preserving kidney function in obese individuals.

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