The prevalence of cardio-metabolic risk factors is differentially elevated in obesity-prone Osborne-Mendel and obesity-resistant S5B/Pl rats.

Life Sci

Department of Physiology, LSU Health Sciences Center, New Orleans, LA 70112, United States of America; Joint Diabetes, Endocrinology & Metabolism Program, Pennington Biomedical Research Center, Baton Rouge, LA 70808, United States of America. Electronic address:

Published: April 2019

Aims: Individual susceptibility to develop obesity may impact the development of cardio-metabolic risk factors that lead to obesity-related comorbid conditions. Obesity-prone Osborne-Mendel (OM) rats expressed higher levels of visceral adipose inflammation than obesity-resistant, S5B/Pl (S5B) rats. However, the consumption of a high fat diet (HFD) differentially affected OM and S5B rats and induced an increase in visceral adipose inflammation in S5B rats. The current study examined the effects of HFD consumption on cardio-metabolic risk factors in OM and S5B rats.

Materials & Methods: Glucose regulation and circulating levels of lipids, adiponectin and C-reactive protein were assessed following 8 weeks of HFD or low fat diet (LFD) consumption. Left ventricle hypertrophy and mRNA expression of cardiovascular disease biomarkers were also quantified in OM and S5B rats.

Key Findings: Circulating levels of triglycerides were higher, while HDL cholesterol, adiponectin and glycemic control were lower in OM rats, compared to S5B rats. In the left ventricle, BNP and CTGF mRNA expression were higher in OM rats and IL-6, IL-1β, VEGF, and iNOS mRNA expression were higher in S5B rats.

Significance: These findings support the hypothesis that cardio-metabolic risk factors are increased in obesity-prone individuals, which may increase the risk for the development of obesity-related comorbidities. In the current models, obesity-resistant S5B rats also exhibited cardiovascular risk factors supporting the importance of monitoring cardiovascular health in individuals characterized as obesity-resistant.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6461046PMC
http://dx.doi.org/10.1016/j.lfs.2019.03.022DOI Listing

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