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Updated: Jun 23, 2026
Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
AT2 receptor deficiency attenuates adipocyte differentiation and decreases adipocyte number in atherosclerotic mice
Masaru Iwai1, Yumiko Tomono, Shinji Inaba
1Department of Molecular Cardiovascular Biology and Pharmacology, Ehime University Graduate School of Medicine, Shitsukawa, Ehime, Japan.
Background:
Previous reports indicated that blockade of AT(1) receptor stimulation attenuated adipocyte dysfunction. However, the effects of AT(2) receptor stimulation on adipose tissue were not yet clear. In the present study, we examined the adipose tissue dysfunction in atherosclerotic apolipoprotein E knockout (ApoEKO) mice with AT(2) receptor deficiency.
Methods:
Male ApoEKO and AT(2) receptor/ApoE knockout (AT(2)/ApoEKO) mice at 6 weeks of age were treated with a normal diet or a high-cholesterol diet (HCD: 1.25% cholesterol). Markers for adipocyte differentiation and inflammation in adipose tissue were assayed with real-time reverse-transcription-PCR and western blot.
Results:
Compared with ApoEKO mice, AT(2)/ApoEKO mice with a normal diet showed only a decrease in expression of adiponectin and CCAAT/enhancer binding protein delta (C/EBPdelta) in epididymal adipose tissue without changes in body weight, adipose tissue weight, and adipocyte number even at 6 months of age. After HCD for 4 weeks, the weight of both epididymal and retroperitoneal adipose tissue in AT(2)/ApoEKO mice was greater than that in ApoEKO mice without a change in body weight. Plasma concentrations of cholesterol and fatty acids were higher in AT(2)/ApoEKO mice than in ApoEKO mice. In adipose tissue of AT(2)/ApoEKO mice, the adipocyte number was decreased and the expression of peroxisome proliferator-activated receptor gamma (PPARgamma), C/EBPalpha, and aP2 was lower than that in ApoEKO mice, in association with an increase in nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity.
Conclusions:
These results suggest that AT(2) receptor stimulation in adipose tissue is involved in the improvement of adipocyte differentiation and adipose tissue dysfunction in atherosclerotic model.
Insights
AT(2) receptor stimulation improves adipocyte differentiation and adipose tissue dysfunction in atherosclerotic mice. Deficiency in AT(2) receptors exacerbates these issues, highlighting the receptor's protective role.
Area of Science:
- Cardiovascular Research
- Metabolic Syndrome
- Adipose Tissue Biology
Background:
- Previous studies linked AT(1) receptor blockade to improved adipocyte function.
- The role of AT(2) receptor stimulation in adipose tissue remained unclear.
- This study investigated AT(2) receptor's impact on adipose tissue in a mouse model of atherosclerosis.
Purpose of the Study:
- To examine the role of AT(2) receptor deficiency in adipose tissue dysfunction.
- To understand the effects of AT(2) receptor stimulation on adipocyte differentiation and inflammation in atherosclerosis.
Main Methods:
- Atherosclerotic apolipoprotein E knockout (ApoEKO) mice and AT(2) receptor/ApoE knockout (AT(2)/ApoEKO) mice were used.
- Mice were fed either a normal or high-cholesterol diet (HCD).
- Adipose tissue markers of differentiation and inflammation were analyzed using RT-PCR and Western blot.
Main Results:
- AT(2)/ApoEKO mice showed reduced adiponectin and C/EBPdelta expression on a normal diet.
- Following HCD, AT(2)/ApoEKO mice exhibited increased adipose tissue weight, plasma cholesterol, and fatty acids.
- AT(2) receptor deficiency led to decreased adipocyte number and altered expression of key adipogenic and inflammatory markers, with increased NADPH oxidase activity.
Conclusions:
- AT(2) receptor stimulation plays a role in enhancing adipocyte differentiation.
- AT(2) receptor signaling contributes to mitigating adipose tissue dysfunction in an atherosclerotic context.
- Targeting AT(2) receptors may offer a therapeutic strategy for metabolic complications in atherosclerosis.
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