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Leptin regulates ACE activity in mice.

Aline Mourao Hilzendeger1, Rafael Leite Morais, Mihail Todiras

  • 1Department of Biophysics, Escola Paulista de Medicina, Federal University of São Paulo, 04023-062 São Paulo, SP, Brazil.

Journal of Molecular Medicine (Berlin, Germany)
|July 9, 2010
PubMed
Summary
This summary is machine-generated.

Leptin deficiency in obese mice reduces angiotensin-I converting enzyme (ACE) activity, impacting blood pressure regulation. Leptin replacement therapy partially restores ACE function, suggesting a link between leptin, ACE, and metabolic syndrome.

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Area of Science:

  • Endocrinology
  • Cardiovascular Physiology
  • Metabolic Syndrome Research

Background:

  • Leptin, a key metabolic hormone, influences blood pressure through incompletely understood mechanisms.
  • Angiotensin-I converting enzyme (ACE) is crucial for cardiovascular function and linked to metabolism and obesity.
  • Obesity and diabetes are associated with altered cardiovascular regulation, but the specific role of ACE and leptin remains unclear.

Purpose of the Study:

  • To investigate the potential interaction between leptin and the renin-angiotensin system (RAS) in regulating blood pressure.
  • To determine if ACE activity is altered in leptin-deficient obese mice (ob/ob) and if leptin influences this.
  • To explore the link between the leptinergic system, RAS, and the pathogenesis of obesity and hypertension.

Main Methods:

  • Utilized ob/ob mice, a model of leptin deficiency, to assess ACE activity, mRNA expression, and blood pressure responses.
  • Administered enalapril (an ACE inhibitor) and infused leptin to evaluate functional changes in the RAS.
  • Measured plasma concentrations of various RAS components, including renin, angiotensinogen, angiotensin I, angiotensin II, and bradykinin.

Main Results:

  • Ob/ob mice exhibited significantly decreased plasma and lung ACE activities and ACE mRNA expression.
  • The hypotensive effect of enalapril was attenuated in obese mice, and leptin infusion partially restored ACE activity.
  • Leptin treatment increased plasma renin activity and angiotensin II in both wild-type and ob/ob mice, with a more pronounced effect on ACE activity in ob/ob mice.

Conclusions:

  • The renin-angiotensin system is altered in leptin-deficient obese mice, characterized by reduced ACE activity.
  • Findings suggest a significant interplay between the angiotensinergic and leptinergic systems.
  • This interaction may contribute to the pathophysiology of obesity, hypertension, and metabolic syndrome.