Abstract
Background
Visceral obesity is associated with diabetogenic and atherogenic abnormalities, including
insulin resistance and increased risk for cardiometabolic diseases and mortality.
Rodent lipectomy studies have demonstrated a causal link between visceral fat and
insulin resistance, yet human omentectomy studies have failed to replicate this metabolic
benefit, perhaps owing to the inability to target the mesentery.
Objectives
We aimed to demonstrate that safe and effective removal of mesenteric fat could be
achieved in obese insulin-resistant baboons using tissue liquefaction technology.
Setting
Southwest National Primate Research Center, San Antonio, Texas.
Methods
Tissue liquefaction technology has been developed to enable mesenteric visceral lipectomy
(MVL) to be safely performed without disturbing the integrity of surrounding nerves
and vessels in the mesentary. After an initial MVL optimization study (n = 3), we
then performed MVL (n = 4) or sham surgery (n = 2) in a cohort of insulin-resistant
baboons, and the metabolic phenotype was assessed via hyperinsulinemic-euglycemic
clamps at baseline and 6 weeks later.
Results
MVL led to a 75% improvement in glucose disposal at 6-weeks follow-up (P = .01). Moreover, despite removing only an average of 430 g of mesenteric fat (~1%
of total body mass), MVL led to a 14.4% reduction in total weight (P = .001). Thus, these data demonstrate that mesenteric fat can be safely targeted
for removal by tissue liquefaction technology in a nonhuman primate, leading to substantial
metabolic improvements, including reversal of insulin resistance and weight loss.
Conclusions
These data provide the first demonstration of successful adipose tissue removal from
the mesentery in a mammal. Importantly, we have demonstrated that when MVL is performed
in obese, insulin-resistant baboons, insulin resistance is reversed, and significant
weight loss occurs. Therefore, trials performing MVL in humans with abdominal obesity
and related metabolic sequelae should be explored as a potential clinical tool to
ameliorate insulin resistance and treat type 2 diabetes.
Keywords
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Article info
Publication history
Published online: March 08, 2018
Accepted:
March 4,
2018
Received:
January 24,
2018
Footnotes
M. S. A. and D. M. H equally contributed to this work.
☆Supported by National Institutes of Health Grant R43 DK112428.
Identification
Copyright
© 2018 American Society for Metabolic and Bariatric Surgery. Published by Elsevier Inc. All rights reserved.
