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Am J Physiol Endocrinol Metab (August 1, 2006). doi:10.1152/ajpendo.00163.2006
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Submitted on April 5, 2006
Accepted on July 11, 2006

Effects of transgenic expression of HIV-1 viral protein R (Vpr) on lipid and energy metabolism in mice

Ashok Balasubramanyam1*, Harry J. Mersmann2, Farook Jahoor3, Terry M Phillips4, Rajagopal V. Sekhar5, Ulrich Schubert6, Baljinder Brar1, Dinakar Iyer1, E. O'Brian Smith7, Hideko Takahashi8, Huiyan Lu9, Peter Anderson10, Tomoshige Kino11, Peter Henklein12, and Jeffrey B Kopp9

1 Division of Diabetes, Endocrinology and Metabolism, Baylor College of Medicine, Houston, Texas, United States
2 USDA/ARS - Department of Pediatrics, Baylor College of Medicine, Houston,, Texas, United States
3 Children's Nutritional Research Center, Baylor College, Houston, Texas, United States; USDA/ARS - Department of Pediatrics, Baylor College of Medicine, Houston,, Texas, United States
4 ORS / OD, NIH, Bethesda, Maryland, United States
5 Division of Diabetes, Endocrinology and Metabolism, Baylor College of Medicine, Houston, Texas, United States; Diabetes, Endocrinology, Metab, Baylor College of Medicine, Houston, Texas, United States
6 Institute of Virology, University of Erlangen, Erlangen, Germany
7 Pediatrics, Baylor College of Medicine, Houston, Texas, United States; USDA/ARS - Department of Pediatrics, Baylor College of Medicine, Houston,, Texas, United States
8 Kidney Disease Section, NIDDK, NIH, Bethesda, Maryland, United States
9 NIDDK, NIH, Bethesda, Maryland, United States
10 Clinical Pharmacy, University of Colorado Health Sciences Center, Denver, Colorado, United States
11 NICHD, NIH, Bethesda, Maryland, United States
12 Institute of Biochemistry, Humboldt University, Berlin, Germany

* To whom correspondence should be addressed. E-mail: ashokb{at}bcm.tmc.edu.

HIV infection is associated with abnormal lipid metabolism, body fat redistribution and altered energy expenditure. The pathogenesis of these complex abnormalities is unclear. Vpr, a HIV-1 accessory protein, can regulate gene transcription mediated by the glucocorticoid receptor and peroxisome proliferator activator receptor-{gamma}, and affect mitochondrial function, in vitro. To test the hypothesis that expression of Vpr in liver and adipocytes can alter lipid metabolism in vivo, we engineered mice to express Vpr under control of the phosphoenolpyruvate carboxykinase promoter in a tissue-specific and inducible manner, and investigated the effects of dietary fat, indinavir and dexamethasone on energy metabolism and body composition. The transgenic mice expressed Vpr mRNA in white and brown adipose tissues and liver, and immunoaffinity capillary electrophoresis revealed that they had free Vpr protein in the plasma. Compared to wild-type (WT) animals, Vpr mice had lower plasma triglyceride levels after 6 weeks (P<0.05) but not after 10 weeks of high fat diet, and lower plasma cholesterol levels after 10 weeks of high fat diet (P<0.05). Treatment with dexamethasone obviated group differences, while indinavir had no significant independent effect on lipids. In the fasted state, Vpr mice had a higher respiratory quotient than WT mice (P<0.05). These data provide the first in vivo evidence that HIV-1 Vpr expressed at low levels in adipose tissues and liver can a) circulate in the blood, b) regulate lipid and fatty acid metabolism, and c) alter fuel selection for oxidation in the fasted state.




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 J. Gen. Virol.Home page
B. Romani and S. Engelbrecht
Human immunodeficiency virus type 1 Vpr: functions and molecular interactions
J. Gen. Virol., August 1, 2009; 90(8): 1795 - 1805.
[Abstract] [Full Text] [PDF]


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