Cited by 71Adipose Tissue and MetabolismAdipokines, Inflammation, and Metabolic DiseasesMitochondrial Function and Pathology

Prohibitin overexpression in adipocytes induces mitochondrial biogenesis, leads to obesity development, and affects glucose homeostasis in a sex-specific manner

Ande, Sudharsana R., Nguyen, K. Hoa, Padilla-Meier, G. Pauline, Wahida, Wahida, Nyomba, B.L. Grégoire, Mishra, Suresh·2014·Diabetes

Abstract

Adipocytes are the primary cells in the body that store excess energy as triglycerides. To perform this specialized function, adipocytes rely on their mitochondria; however, the role of adipocyte mitochondria in the regulation of adipose tissue homeostasis and its impact on metabolic regulation is not understood. We developed a transgenic mouse model, Mito-Ob, overexpressing prohibitin (PHB) in adipocytes. Mito-Ob mice developed obesity due to upregulation of mitochondrial biogenesis in adipocytes. Of note, Mito-Ob female mice developed more visceral fat than male mice. However, female mice exhibited no change in glucose homeostasis and had normal insulin and high adiponectin levels, whereas male mice had impaired glucose homeostasis, compromised brown adipose tissue structure, and high insulin and low adiponectin levels. Mechanistically, we found that PHB overexpression enhances the cross talk between the mitochondria and the nucleus and facilitates mitochondrial biogenesis. The data suggest a critical role of PHB and adipocyte mitochondria in adipose tissue homeostasis and reveal sex differences in the effect of PHB-induced adipocyte mitochondrial remodeling on whole-body metabolism. Targeting adipocyte mitochondria may provide new therapeutic opportunities for the treatment of obesity, a major risk factor for type 2 diabetes.

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Crossref · 10.2337/db13-1807

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  • Overexpression of prohibitin in adipocytes produces development of obesity in mice accompanied by induction of mitochondrial biogenesis.

    “overexpression of prohibitin in adipocytes produces the development of obesity in mice accompanied by the induction of mitochondrial biogenesis (Ande et al., 2014).”

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Authors
Ande, S. R., Nguyen, K. H., Padilla-Meier, G. P., Wahida, W., Nyomba, B. L. G., & Mishra, S.
Affiliations
  • University of Manitoba (CA)
  • Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
Corresponding author
Mishra, Suresh
Venue
Diabetes
Published
2014-10-13
Volume
63
Issue
11
Pages
3734-3741
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
OpenAlex
W2157955877
Cited by
71
References
26
Citations by year
2026: 4 · 2025: 7 · 2024: 5 · 2023: 6 · 2022: 8 · 2021: 5 · 2020: 6 · 2019: 6 · 2018: 6 · 2017: 7 · 2016: 8 · 2015: 3
FWCI
3.99
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
prohibitin, adipocytes, mitochondrial biogenesis, obesity, glucose homeostasis, sex differences, adipose tissue homeostasis, brown adipose tissue, nuclear-mitochondrial crosstalk, adiponectin, insulin, type 2 diabetes, transgenic mouse model
MeSH terms
Prohibitins, Animals, Diabetes Mellitus, Type 2, Female, Glucose, Homeostasis, Insulin, Male, Mice, Transgenic, Obesity, Repressor Proteins, Sex Factors, Adipocytes, Mice, Adiponectin, Mitochondrial Turnover

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