Related Experiment Video

Updated: Mar 14, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

10.6K

Caveolin 1 Modulates Aldosterone-Mediated Pathways of Glucose and Lipid Homeostasis

Rene Baudrand1, Nidhi Gupta2, Amanda E Garza2

  • 1Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA Department of Endocrinology, School of Medicine, Pontificia Universidad Catolica De Chile, Santiago, Chile.

Journal of the American Heart Association
|September 30, 2016
PubMed
Abstract

Insights

Reduced caveolin 1 (cav-1) expression may worsen insulin resistance and dyslipidemia by enhancing aldosterone signaling. This study investigated the link between cav-1 and aldosterone in mice and humans, finding decreased cav-1 exacerbates these conditions.

Area of Science:

  • Endocrinology
  • Metabolic Syndrome
  • Genetics

Background:

  • Aldosterone and mineralocorticoid receptor (MR) pathway overactivation is linked to hyperglycemia and dyslipidemia.
  • Caveolin 1 (cav-1) plays a role in glucose/lipid homeostasis and may influence MR signaling.

Purpose of the Study:

  • To investigate the interplay between cav-1 and aldosterone signaling in insulin resistance and dyslipidemia.
  • To examine these effects in both cav-1-null mice and humans with a common CAV1 gene variant.

Main Methods:

  • Studied cav-1 knockout mice and analyzed the CAV1 gene polymorphism rs926198 in 556 human participants.
  • Assessed insulin resistance, lipid profiles, resistin levels, and gene expression.
  • Investigated the effects of MR blockade with eplerenone in mice.

Main Results:

  • Cav-1 knockout mice showed increased insulin resistance, cholesterol, resistin, and hypertriglyceridemia.
  • MR blockade in mice reduced glycemia, cholesterol, and resistin but not insulin or triglycerides.
  • Human carriers of the minor CAV1 allele (rs926198) had higher odds of insulin resistance and low HDL, with aldosterone correlating with these markers.

Conclusions:

  • Decreased cav-1 expression may potentiate aldosterone/MR signaling effects on glycemia, dyslipidemia, and resistin.
  • Hyperinsulinemia and hypertriglyceridemia appear to be mediated by MR-independent pathways.
  • Further research is needed to clarify the clinical relevance of MR blockade in individuals with genotype-mediated cav-1 deficiency.
Keywords:
aldosteronecaveolin 1dyslipidemiaeplerenoneinsulin resistancemineralocorticoid receptor

More Related Videos

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro09:41

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro

Published on: March 17, 2023

3.9K
Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy08:47

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy

Published on: December 7, 2017

10.3K

Related Concept Videos

Glucose Homeostasis: Regulation of Blood Glucose01:02

Glucose Homeostasis: Regulation of Blood Glucose

Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
5.0K
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
8.9K
Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

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.
In addition to accelerating glucose uptake and utilization, insulin has...
8.1K
Glucose Absorption Into the Small Intestine01:26

Glucose Absorption Into the Small Intestine

Complex carbohydrates consumed cannot be absorbed into the small intestine in their original form. First, they must be hydrolyzed to a monosaccharide form such as glucose or galactose. These monosaccharides are then transported across the intestinal membrane and into the blood via transcellular transport. The intestinal epithelial cells allow the movement of these monosaccharides with a defined 'entry' through membrane transporter proteins present on their apical membrane and...
36.9K
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
8.0K
Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
7.2K