Sexual dimorphism,weight gain and glucose intolerance in a B- and T-cell deficient mouse model |
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| Institution: | 1. Department of Pharmacy Practice, School of Pharmacy and Pharmaceutical Sciences, State University of New York at Buffalo, Buffalo, NY, USA;2. Department of Math and Natural Sciences, D’Youville College, Buffalo, NY, USA;3. Department of Clinical Pathology, Roswell Park Cancer Institute, Buffalo, NY, USA;1. Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, Huazhong Agricultural University, Wuhan, People''s Republic of China;2. Laboratory of Sheep and Goat Genetics, Breeding and Reproduction, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan, People''s Republic of China;1. Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research, Olsztyn, Poland;2. C.I.I.S.A., Faculty of Veterinary Medicine, University of Lisbon, Lisbon, Portugal;1. Medical Biochemistry Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt;2. Pediatrics Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt;1. State Key Laboratory of Veterinary Etiological Biology, Key Laboratory of Veterinary Parasitology of Gansu Province, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, Gansu Province 730046, PR China;2. Department of Infectious Diseases, Clinical Institute, and Institute of Medical Microbiology and Immunology, Faculty of Health Sciences, Aarhus University, Aarhus, Denmark;3. College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University, Daqing, Heilongjiang Province 163319, PR China;1. Department of Animal and Food Sciences, Texas Tech University, Lubbock, TX 79409-2141, USA;2. Department of Pathology, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA;3. Animal Biotech, Dallas, TX 75201, USA;4. Department of Biology, South Plains College, Levelland, TX 79336, USA |
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| Abstract: | BackgroundEstrogen 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.MethodsA 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.ResultsUnlike 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).ConclusionsThe 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. |
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| Keywords: | Sexual dimorphism Adaptive immune system Insulin resistance Estrogen Adipokines |
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