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Sexual dimorphism, weight gain and glucose intolerance in a B- and T-cell deficient mouse model.

Wintrob ZA1, Oppong EK1, Foster M1, Martorana M2, Tse YC1, Zhong L1, Welt JM1, Boateng HR1, Drumea IM1, Irlam J3, Levea CM3, Faitar SL2, Ceacareanu AC4.

Cytokine. 2014 ;67(2):102-6.

 

1Department of Pharmacy Practice, School of Pharmacy and Pharmaceutical Sciences, State University of New York at Buffalo, Buffalo, NY, USA.

2Department of Math and Natural Sciences, D’Youville College, Buffalo, NY, USA.

3Department of Clinical Pathology, Roswell Park Cancer Institute, Buffalo, NY, USA.

4Department of Pharmacy Practice, School of Pharmacy and Pharmaceutical Sciences, State University of New York at Buffalo, Buffalo, NY, USA. Electronic address: [email protected]

 

Abstract

BACKGROUND:

Estrogen is thought to aid maintenance of insulin sensitivity potentially through modulation of a counter-regulatory mechanism that interferes with the contribution of adaptive and innate immune systems to visceral fat deposition. We evaluated the impact of estrogen on long-term high fat diet (HFD) intake in B- and T-cell deficient and immunocompetent animals comparatively.

METHODS:

A total of 16 BALB and 16 SCID mice, 8 of each sex and strain, were randomized to receive low fat diet, 4.1% fat or HFD, 35% fat, such that there was a group of both each sex and each strain receiving each diet. Biweekly levels of adiponectin, leptin and insulin levels were assessed and a glucose tolerance test (GTT) was performed after 13 weeks.

RESULTS:

Unlike their male counterparts, HFD-fed SCID females neither gained weight, nor became insulin resistant. Meanwhile, in the HFD-fed BALB groups both males and females gained weight similarly, but remarkable  sexual dimorphism was nonetheless observed. The females had notable higher adiponectin levels as compared to males (10-60 μg/mL vs. 6-10 μg/mL respectively) causing the adiponectin-to-leptin (A/L) ratio to reach 80 one week after HFD initiation. The A/L dropped to 10, still higher than males, by week 13, but dropped to 2 by the end of the study in agreement with inverse insulin trends. None of the HFD-fed female groups developed insulin resistance (IR) by week 13, while all male counterparts had. Similar results were observed in the HFD-fed SCID groups whereby the females did not develop IR and had a higher A/L; however, adiponectin levels were comparable between groups (5-11 μg/mL).

CONCLUSIONS:

The present study provides lacking evidence indicating that estrogen may be sufficient to prevent weight gain and development of glucose intolerance in high-fat fed B- and T-cell deficient mice.

Copyright © 2014 Elsevier Ltd. All rights reserved.

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