title: Removal of intra-abdominal visceral adipose tissue improves glucose tolerance in rats: role of hepatic triglyceride storage.
abstract: Epidemiological studies have demonstrated a strong link between increased visceral fat and metabolic syndrome. In rodents, removal of intra-abdominal but non-visceral fat improves insulin sensitivity and glucose homeostasis, though previous studies make an imprecise comparison to human physiology because actual visceral fat was not removed. We hypothesize that nutrient release from visceral adipose tissue may have greater consequences on metabolic regulation than nutrient release from non-visceral adipose depots since the latter drains into systemic but not portal circulation. To assess this we surgically decreased visceral white adipose tissue (~0.5 g VWATx) and compared the effects to removal of non-visceral epididymal fat (~4 g; EWATx), combination removal of visceral and non-visceral fat (~4.5 g; EWATx/VWATx) and sham-operated controls, in chow-fed rats. At 8 weeks after surgery, only the groups with visceral fat removed had a significantly improved glucose tolerance, although 8 times more fat was removed in EWATx compared with VWATx. This suggests that mechanisms controlling glucose metabolism are relatively more sensitive to reductions in visceral adipose tissue mass. Groups with visceral fat removed also had significantly decreased hepatic lipoprotein lipase (LPL) and triglyceride content compared with controls, while carnitine palmitoyltransferase (CPT-1A) was decreased in all fat-removal groups. In a preliminary experiment, we assessed the opposite hypothesis; i.e., we transplanted excess visceral fat from a donor rat to the visceral cavity (omentum and mesentery), which drains into the hepatic portal vein, of a recipient rat but observed no major metabolic effect. Overall, our results indicate surgical removal of intra-abdominal fat improves glucose tolerance through mechanism that may be mediated by reductions in liver triglyceride.
authors.affiliation: Obesity Research Center, Department of Psychiatry, University of Cincinnati, Cincinnati, OH 45237, United States. Michelle.Foster@uc.edu
authors.forename: Michelle T
authors.initials: MT
authors.lastname: Foster
authors.forename: Haifei
authors.initials: H
authors.lastname: Shi
authors.forename: Randy J
authors.initials: RJ
authors.lastname: Seeley
authors.forename: Stephen C
authors.initials: SC
authors.lastname: Woods
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D019540:Area Under Curve; D001786:Blood Glucose; D001823:Body Composition / Q000187:drug effects; D015992:Body Mass Index; D005786:Gene Expression Regulation / Q000502:physiology; D005947:Glucose / Q000008:administration & dosage; D005951:Glucose Tolerance Test; D007328:Insulin / Q000008:administration & dosage; D007333:Insulin Resistance; D050152:Intra-Abdominal Fat / Q000502:physiology* / Q000601:surgery* / Q000637:transplantation; D008099:Liver / Q000378:metabolism*; D008297:Male; D051381:Rats; D020318:Rats, Long-Evans; D014280:Triglycerides / Q000235:genetics / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D007328:Insulin; D014280:Triglycerides; D005947:Glucose