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Enhancing enterocyte fatty acid oxidation in mice affects glycemic control depending on dietary fat.

Scientific reports (2018-07-19)
Deepti Ramachandran, Rosmarie Clara, Shahana Fedele, Ladina Michel, Johannes Burkard, Sharon Kaufman, Abdiel Alvarado Diaz, Nadja Weissfeld, Katrien De Bock, Carina Prip-Buus, Wolfgang Langhans, Abdelhak Mansouri
ABSTRACT

Studies indicate that modulating enterocyte metabolism might affect whole body glucose homeostasis and the development of diet-induced obesity (DIO). We tested whether enhancing enterocyte fatty acid oxidation (FAO) could protect mice from DIO and impaired glycemic control. To this end, we used mice expressing a mutant form of carnitine palmitoyltransferase-1a (CPT1mt), insensitive to inhibition by malonyl-CoA, in their enterocytes (iCPT1mt) and fed them low-fat control diet (CD) or high-fat diet (HFD) chronically. CPT1mt expression led to an upregulation of FAO in the enterocytes. On CD, iCPT1mt mice had impaired glycemic control and showed concomitant activation of lipogenesis, glycolysis and gluconeogenesis in their enterocytes. On HFD, both iCPT1mt and control mice developed DIO, but iCPT1mt mice showed improved glycemic control and reduced visceral fat mass. Together these data indicate that modulating enterocyte metabolism in iCPT1mt mice affects glycemic control in a body weight-independent, but dietary fat-dependent manner.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Monoclonal Anti-β-Actin antibody produced in mouse, clone AC-74, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
Trypsin inhibitor from Glycine max (soybean), solution, sterile-filtered, suitable for, suitable for cell culture