alexa Insulin and Testosterone are Associated with Elevated Intestinal Secretion of Lipids and Lipoproteins in a Rodent Model of the Metabolic and Polycystic Ovary Syndrome
ISSN: 2155-6156

Journal of Diabetes & Metabolism
Open Access

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Research Article

Insulin and Testosterone are Associated with Elevated Intestinal Secretion of Lipids and Lipoproteins in a Rodent Model of the Metabolic and Polycystic Ovary Syndrome

Donna F Vine*, Ye Wang, Danni Shi and Spencer D Proctor

Metabolic and Cardiovascular Disease Laboratory, University of Alberta, Edmonton, Alberta, Canada

*Corresponding Author:
Donna Vine
Metabolic and Cardiovascular Disease Laboratory
Alberta Institute for Human Nutrition, Alberta Diabetes Institute
4-002 Li Ka- Shing Centre for Health Research Innovation
University of Alberta, Edmonton, Alberta, Canada
Tel: 780-492-4393
Fax: +1 780 4929270
Email: [email protected]

Received date: May 08, 2014; Accepted date: June 09, 2014; Published date: June 17, 2014

Citation: Vine DF, Wang Y, Shi D, Proctor SD (2014) Insulin and Testosterone are Associated with Elevated Intestinal Secretion of Lipids and Lipoproteins in a Rodent Model of the Metabolic and Polycystic Ovary Syndrome. J Diabetes Metab 5:391. doi: 10.4172/2155-6156.1000391

Copyright: © 2014 Vine D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use,distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

The metabolic syndrome is highly associated with the incidence of Polycystic Ovary Syndrome (PCOS). The metabolic aberrations of insulin resistance and hyperandrogenemia have been proposed to contribute to the development of dyslipidemia and increased Cardiovascular Disease (CVD) risk in PCOS. The contribution of nonfasting intestinal lipemia to CVD risk is well established, however little is known regarding the role of androgens in regulating these pathways in conditions of the metabolic syndrome and PCOS. The aim of this study was to determine the contribution of the intestine to lipemia, and the relationship with serum testosterone and insulin in the JCR: LA-cp rodent model of the metabolic syndrome and PCOS. Fasting and non-fasting plasma lipid and intestinal apolipoprotein (apo) B- metabolism were measured in the fasting state, and non-fasting state in response to a highfat meal. In addition, intestinal mesenteric lymph cannulation was used to determine the intestinal secretion of apoBlipoproteins and associated lipids. The PCOS-like genotype was observed to have elevated fasting and non-fasting plasma triglyceride, cholesterol and apo-B48 (a marker of intestinal-derived apoB-lipoproteins) compared to control animals. Intestinal lymphatic secretion of apoB48-lipoproteins, triglyceride and cholesterol were elevated in the fasted and non-fasted state. Serum total testosterone and insulin were shown to be positively correlated with fasting and non-fasting plasma triglyceride and apoB48 concentrations. In conclusion, the intestinal oversecretion of apo- B48 lipoproteins and lipids contributes to dyslipidemia in the JCR: LA-cp rodent model of the metabolic syndrome and PCOS. This model may be used to further our understanding of the pathophysiology of dyslipidemia and CVD risk in conditions of hyperandrogenemia and insulin resistance in PCOS.

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