Body mass recovery after visceral lipectomy improves glucose tolerance without adipose recovery in obese, insulin resistant rats.
Authors: Cornejo Manuel Alejandro , Emery Janna , Smith Megan , Nishiyama Akira , Nakano Daisuke , Ortiz Rudy Martin 
Published: April 2020

Increased visceral fat is associated with metabolic dysregulation, which may be a consequence of chronic exposure of the liver to adipokines and fatty acids derived from visceral adipose, increased hepatic glucose output, and insulin resistance. Therefore, lipectomy (rapid removal of adipose) may ameliorate insulin resistance and other associated maladies. However, abdominal lipectomy did not significantly improve insulin resistance in obese, non‐diabetic females studied one year after their surgery. Moreover, in Sprague‐Dawley rats, fasting glucose and plasma leptin and insulin increased and lipogenesis was stimulated 10 days after lipectomy suggesting that maladaptation may be a consequence of lipectomy. We have previously demonstrated that 50% caloric restriction for 10 days (gradual reduction in adiposity) decreased visceral fat 2.1% associated with an improvement in insulin resistance index and triglyceridemia in OLETF rats. Our goal was to assess the effects of visceral lipectomy (rapid loss) with fat removal comparable to the adipose lost (gradual) in our previous study, with and without mass recovery, in a model of metabolic syndrome.Sixteen lean LETO and 32 obese, insulin resistant OLETF rats were weighted daily (Fig.
) and fed ad libidum until 18 weeks of age. OLETF rats (n=18) were subjected to removal of retroperitoneal and epididymal fat equivalent to 2 ± 0.1% of their total body mass, while the rest of the rats were subjected to sham surgery. Half of sham LETO and OLETF (Lpx Ctrl), and half of the lipectomized rats (OLETF Lpx) were subjected to oGTT two days after surgery and dissected 3 days later. The rest of the groups (LETO, OLETF Rec Ctrl, and OLETF Rec), were subjected to oGTT 10 days after surgery and dissected 3 days later.Mean glucose AUC (mg*h/dL) was 2‐fold higher in OLETF vs LETO at 18 w.o. (669 ± 39 vs 332 ± 9, P=0.428). Glucose AUC did not change in OLETF Lpx compared to control (726 ± 73 vs 669 ± 39, P=0.428), however it decreased 28% after mass recovery (408 ± 7 vs 570 ± 52, P=0.044) (Fig.
). Visceral (epididimal + retroperitoneal) relative mass did not increase with age in OLETF (6.8 ± 0.2% vs 6.2 ± 0.2% at 19 and 20 w.o, respectively). Moreover, relative mass decreased in OLETF Rec compared to OLETF Lpx (3.7 ± 0.5 vs 5.0 ± 0.2%, P<0.001) despite an increase in total body mass (Lpx: 508 ± 12 vs Rec: 538 ± 24 g). We conclude that glucose tolerance was improved after body mass recovery without recovery of the retroperitoneal or epididymal depots, reaffirming the role of visceral fat in insulin resistance.Support or Funding InformationThis research was supported in part by the University of California Institute for Mexico and the United States and Mexico’s National Council for Science and Technology doctoral fellowship UC MEXUS‐CONACYT 440553 and by National Institute on Minority Health and Health Disparities grant 9T37‐MD001480Mean ± SE body mass (g). After surgery, mass was not recorded until the day after oGTT, two days before dissection.Figure 1Mean ± SE glucose AUC (mg*h/dl). aP<0.05 vs LETO, bP<0.05 vs Ctrl, cP<0.05 vs LpxFigure 2