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Obesity (Silver Spring). 2007 Jul;15(7):1675-84.

Trans fat diet induces abdominal obesity and changes in insulin sensitivity in monkeys.

Author information

1
Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA. kkavanag@wfubmc.edu

Abstract

OBJECTIVE:

There is conflicting evidence about the propensity of trans fatty acids (TFAs) to cause obesity and insulin resistance. The effect of moderately high intake of dietary monounsaturated TFAs on body composition and indices of glucose metabolism was evaluated to determine any pro-diabetic effect in the absence of weight gain.

RESEARCH METHODS AND PROCEDURES:

Male African green monkeys (Chlorocebus aethiops; n=42) were assigned to diets containing either cis-monounsaturated fatty acids or an equivalent diet containing the trans-isomers (approximately 8% of energy) for 6 years. Total calories were supplied to provide maintenance energy requirements and were intended to not promote weight gain. Longitudinal body weight and abdominal fat distribution by computed tomography scan analysis at 6 years of study are reported. Fasting plasma insulin, glucose, and fructosamine concentrations were measured. Postprandial insulin and glucose concentrations, and insulin-stimulated serine/threonine protein kinase (Akt), insulin receptor activation, and tumor necrosis factor-alpha concentrations in subcutaneous fat and muscle were measured in subsets of animals.

RESULTS:

TFA-fed monkeys gained significant weight with increased intra-abdominal fat deposition. Impaired glucose disposal was implied by significant postprandial hyperinsulinemia, elevated fructosamine, and trends toward higher glucose concentrations. Significant reduction in muscle Akt phosphorylation from the TFA-fed monkeys suggested a mechanism for these changes in carbohydrate metabolism.

DISCUSSION:

Under controlled feeding conditions, long-term TFA consumption was an independent factor in weight gain. TFAs enhanced intra-abdominal deposition of fat, even in the absence of caloric excess, and were associated with insulin resistance, with evidence that there is impaired post-insulin receptor binding signal transduction.

PMID:
17636085
DOI:
10.1038/oby.2007.200
[Indexed for MEDLINE]
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