Body composition and cardiometabolic disease risk factors in captive baboons (Papio hamadryas sp.): Sexual dimorphism

Abstract

Baboons (Papio hamadryas Sp.) exhibit significant sexual dimorphism in body size. Sexual dimorphism is also exhibited in a number of circulating factors associated with risk of cardiometabolic disease. We investigated whether sexual dimorphism in body size and composition underlie these differences. We examined data from 28 male and 24 female outdoor group-housed young adult baboons enrolled in a longitudinal observational study of cardiometabolic disease risk factors. Animals were sedated with ketamine HCl (10mg/Kg) before undergoing venous blood draws, basic body measurements, and dual-energy X-ray absorptiometry (DXA) body composition scans. Percentage glycated hemoglobin (%HbA1C) was measured in whole blood. Serum samples were analyzed for glucose, insulin, C-peptide, HDL-, and triglyceride concentrations. Males were heavier and had greater body length and lean tissue mass than females. Females had a greater body fat percentage relative to males (10.8 ±6.4 vs. 6.9 ±4.0, P=0.01). Although C-peptide, fasting glucose, and %HbA1C did not differ between the sexes, females had greater fasting insulin and triglyceride compared to their male counterparts. Insulin and percentage body fat were significantly correlated in males (r=0.61, P=0.001) and to a lesser extent in females (r=0.43, P=0.04). Overall, relations between adiposity and fasting insulin and fasting triglyceride were stronger in males. After accounting for differences in percentage body fat, fasting insulin and triglyceride were no longer statistically different between males and females. Despite stronger correlations between relative adiposity and insulin and triglyceride in males, the higher fasting insulin and triglyceride of female baboons may be underlain by their greater relative body fat masses.

Nonhuman Primates and Translational Research—Cardiovascular Disease

“…In addition, a diet high in simple carbohydrates and fat causes baboons to develop increased body fat and TG concentrations, altered adipokine concentrations, and altered glucose metabolism, consistent with observations in humans (Higgins et al 2010). Even on a normal chow diet, some animals develop insulin resistance, dyslipidemia, atherosclerosis, and CVD, recapitulating metabolic complications seen in humans (Higgins et al 2014;Kamath et al 2011;Kulkarni et al 2014).…”

Central GIP signaling stimulates peripheral GIP release and promotes insulin and pancreatic polypeptide secretion in nonhuman primates

“…Given the particular importance of nonhuman primates as translational models for metabolic diseases (7, 40), investigations to confirm that gut-brain and brain-gut signaling pathways found in rodents are operative in nonhuman primates is of considerable importance. The baboon model is well established in the study of all stages of metabolic disease (9,19,25,26,28,46). Our ICV infusion methodology advances previously described ICV infusion techniques applied in conscious nonhuman primates (3,4,43).…”

Duodenal adipose tissue is associated with obesity in baboons (Papio sp): a novel site of ectopic fat deposition in non-human primates

“…Taken together, the correlations suggest that circulating leptin, adiponectin, and triglyceride concentrations were more strongly related to %DFAT than to AC. Although we were limited to the use of AC as a measure of whole body adiposity, we have previously shown that AC is a robust predictor of dual-energy X-ray absorptiometry measured body fat in baboons [16,28] as both male and female baboons distribute excess body fat in the abdominal region [15]. However, we have previously shown that whole body fat deposition negatively affects insulin sensitivity determined by the gold standard methodology, the euglycemic clamp as well as indirect measures of insulin sensitivity such as Homa-IR and insulin levels (16,28).…”

“…housed at the Southwest National Primate Research Center (SNPRC), San Antonio, TX. Female baboons were studied to avoid the confounding effects of sex differences in adiposity and metabolic disease risk factors [15,16].…”