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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #335882
Title: Coconut oil prevents hepatic steatitis but not adipose inflammation in obese mice

Author
item Picklo, Matthew
item Idso, Joseph
item Zeng, Huawei

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/1/2017
Publication Date: 4/1/2017
Citation: Picklo, M.J., Idso, J.P., Zeng, H. 2017. Coconut oil prevents hepatic steatitis but not adipose inflammation in obese mice [abstract]. Journal of Federation of American Societies for Experimental Biology. 31:971.25.

Interpretive Summary:

Technical Abstract: While saturated fat intake is associated with obesity and its comorbidities, there are little data indicating the impact of specific saturated fatty acids (SFA). In particular, data are lacking in which only SFA type, but not other fatty acids, is changed. In this work, we tested the hypothesis that intake of obesogenic diets containing medium chain SFA reduce hepatic steatosis and insulin resistance. Male, C57BL/6J mice were fed obesogenic diets of 48% energy (en) fat (28 % SFA, 14% oleic acid, and 6% polyunsaturated fatty acid) or a control diet with 16% en fat (5% SFA, 4% oleic acid, and 7% PUFA) for 16 weeks. Obesogenic groups were divided by SFA source: coconut oil-based (CCO) with high lauric acid, a palm-oil based (PO) with palmitic acid and stearic acids, and a MIX group with similar levels of the SFAs. All mice eating the obesogenic diets became obese compared to the control group. While all obese animals were insulin resistant, PO animals had higher insulin resistance (assessed by HOMA-IR) than CCO and MIX animals. Hepatic triacylglycerides (TAG) were elevated in the PO and MIX groups, but not the CCO group. The accumulation of hepatic lipid was confirmed with histological analysis. Hepatic expression of the inflammatory cytokine MCP-1 was elevated by intake of the PO diet, but not the CCO and MIX diets. On the other hand, expression of MCP-1 and TNF alpha in visceral adipose was elevated by all three obesogenic diets. Hepatic protein levels of stearoyl-CoA desaturase 1(SCD-1), fatty acid synthase (FASN), but not acetyl CoA carboxylase 1 (ACC1), were reduced by intake of CcO and PO diets. These data indicate that intake of CCO has selective protective effects against hepatic steatosis but not adipose dysfunction. These data indicate a decrease in de novo lipogenesis induced by the obesogenic diets and that perturbation of other processes such as VLDL secretion or fatty acid oxidation impact hepatic TAG deposition and are SFA-type dependent.