Prohibitin has an important role in adipocyte differentiation

Ande, Sudharsana Rao; Xu, Zuyuan; Gu, Yuanyuan; Mishra, Suresh

doi:10.1038/ijo.2011.227

Cited by 57 publications

(73 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The obese phenotype of Mito-Ob mice affirms the emerging notion that PHB and adipocyte mitochondria play a role in the regulation of adipose tissue homeostasis and metabolic regulation (1)(2)(3)(4)(8)(9)(10). However, the metabolic consequences of obesity in Mito-Ob mice are sex specific, suggesting that intrinsic differences exist in the way adipose tissues are regulated and/or respond to obesity development in male and female mice despite a similar underlying cause.…”

Section: Discussionmentioning

confidence: 71%

“…Phb knockdown in Caenorhabditis elegans results in a significant reduction in intestinal fat content (8). Moreover, PHB overexpression in preadipocytes facilitates adipogenesis, whereas PHB silencing attenuates adipogenesis and mitochondrial function (4,9,10). Collectively, this evidence points to a role of PHB in adipose tissue biology; however, the precise mechanism involved remains to be determined.…”

mentioning

confidence: 76%

“…Adipose tissue lysates from Mito-Ob and wild-type mice containing equal amounts of proteins (;15 mg/lane) were separated by SDS-PAGE and subsequently analyzed by immunoblotting (4,13). MitoBiogenesis Western blotting cocktail (Abcam Inc.) was used to determine succinate dehydrogenase-A (SDH-A) and cytochrome c oxidase-I (COX-I) protein levels in adipose tissue.…”

Section: Western Immunoblottingmentioning

confidence: 99%

“…We have reported that prohibitin (PHB [also known as PHB1]) is important in adipocyte differentiation (4). PHB is an evolutionarily conserved protein that functions as a mitochondrial chaperone and plays an important role in mitochondrial biology (5).…”

mentioning

confidence: 99%

See 3 more Smart Citations

Prohibitin Overexpression in Adipocytes Induces Mitochondrial Biogenesis, Leads to Obesity Development, and Affects Glucose Homeostasis in a Sex-Specific Manner

et al. 2014

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 71%

mentioning

confidence: 76%

Section: Western Immunoblottingmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Prohibitin Overexpression in Adipocytes Induces Mitochondrial Biogenesis, Leads to Obesity Development, and Affects Glucose Homeostasis in a Sex-Specific Manner

et al. 2014

View full text Add to dashboard Cite

show abstract

“…PHB1 (51,53), PHB2 (56), and PHB1⅐PHB2 complexes (14,57) associate with plasma membrane lipid rafts that are believed to modulate many intracellular signaling events. Overexpression of PHB1 in 3T3-L1 fibroblasts up-regulates basal ERK MAPK signaling, leading to adipogenesis (58). In contrast, increased PHB1 phosphorylation, rather than changed PHB1 protein levels in lipid rafts, plays an important role in the Ras-driven activation of PIP3/AKT and Raf-1/ERK signaling cascades, resulting in the promotion of cancer cell metastasis (23).…”

Section: Discussionmentioning

confidence: 99%

Prohibitin-2 Binding Modulates Insulin-like Growth Factor-binding Protein-6 (IGFBP-6)-induced Rhabdomyosarcoma Cell Migration

Yang

Bach

2013

Journal of Biological Chemistry

View full text Add to dashboard Cite

Deletion of adipocyte prohibitin 1 exacerbates high‐fat diet‐induced steatosis but not liver inflammation and fibrosis

et al. 2022

View full text Add to dashboard Cite

Adipose tissue dysfunction is closely associated with the development and progression of nonalcoholic fatty liver disease (NAFLD). Recent studies have implied an important role of prohibitin‐1 (PHB1) in adipose tissue function. In the current study, we aimed to explore the function of adipocyte PHB1 in the development and progression of NAFLD. The PHB1 protein levels in adipose tissues were markedly decreased in mice fed a high‐fat diet (HFD) compared to those fed a chow diet. To explore the function of adipocyte PHB1 in the progression of NAFLD, mice with adipocyte‐specific (adipo) deletion of Phb1 (Phb1adipo−/− mice) were generated. Notably, Phb1adipo−/− mice did not develop obesity but displayed severe liver steatosis under HFD feeding. Compared to HFD‐fed wild‐type (WT) mice, HFD‐fed Phb1adipo−/− mice displayed dramatically lower fat mass with significantly decreased levels of total adipose tissue inflammation, including macrophage and neutrophil number as well as the expression of inflammatory mediators. To our surprise, although liver steatosis in Phb1adipo−/− mice was much more severe, liver inflammation and fibrosis were similar to WT mice after HFD feeding. RNA sequencing analyses revealed that the interferon pathway was markedly suppressed while the bone morphogenetic protein 2 pathway was significantly up‐regulated in the liver of HFD‐fed Phb1adipo−/− mice compared with HFD‐fed WT mice. Conclusion: HFD‐fed Phb1adipo−/− mice display a subtype of the lean NAFLD phenotype with severe hepatic steatosis despite low adipose mass. This subtype of the lean NAFLD phenotype has similar inflammation and fibrosis as obese NAFLD in HFD‐fed WT mice; this is partially due to reduced total adipose tissue inflammation and the hepatic interferon pathway.

show abstract

Prohibitin has an important role in adipocyte differentiation

Cited by 57 publications

References 49 publications

Prohibitin Overexpression in Adipocytes Induces Mitochondrial Biogenesis, Leads to Obesity Development, and Affects Glucose Homeostasis in a Sex-Specific Manner

Prohibitin Overexpression in Adipocytes Induces Mitochondrial Biogenesis, Leads to Obesity Development, and Affects Glucose Homeostasis in a Sex-Specific Manner

Prohibitin-2 Binding Modulates Insulin-like Growth Factor-binding Protein-6 (IGFBP-6)-induced Rhabdomyosarcoma Cell Migration

Deletion of adipocyte prohibitin 1 exacerbates high‐fat diet‐induced steatosis but not liver inflammation and fibrosis

Contact Info

Product

Resources

About