Time-restricted feeding mice a high-fat diet induces a unique lipidomic profile

Oct 25, 2020The Journal of nutritional biochemistry

Limited-time eating of a high-fat diet creates a distinct fat molecule pattern in mice

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Abstract

Time-restricted feeding (TRF) of a high-fat diet alters the lipidomic profile of plasma, liver, and adipose tissue.

TRF prevented insulin resistance and hepatic steatosis typically caused by high-fat diet consumption.
Plasma levels of long-chain polyunsaturated fatty acids (LCPUFA) increased with a high-fat diet but were blocked by TRF.
TRF elevated concentrations of triacylglycerols and non-esterified saturated fatty acids in plasma.
Analysis revealed a distinct hepatic lipid signature with changes in triacylglycerols, phosphatidylcholine, and phosphatidylethanolamine species due to TRF.
TRF modified gene and protein expression linked to reduced fatty acid synthesis and restoration of normal gene signaling patterns.

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Time-restricted feeding (TRF) can reduce adiposity and lessen the co-morbidities of obesity. Mice consuming obesogenic high-fat (HF) diets develop insulin resistance and hepatic steatosis, but have elevated indices of long-chain polyunsaturated fatty acids (LCPUFA) that may be beneficial. While TRF impacts lipid metabolism, scant data exist regarding the impact of TRF upon lipidomic composition of tissues. We (1) tested the hypothesis that TRF of a HF diet elevates LCPUFA indices while preventing insulin resistance and hepatic steatosis and (2) determined the impact of TRF upon the lipidome in plasma, liver, and adipose tissue. For 12 weeks, male, adult mice were fed a control diet ad libitum, a HF diet ad libitum (HF-AL), or a HF diet with TRF, 12 hours during the dark phase (HF-TRF). HF-TRF prevented insulin resistance and hepatic steatosis resulting from by HF-AL treatment. TRF-blocked plasma increases in LCPUFA induced by HF-AL treatment but elevated concentrations of triacylglycerols and non-esterified saturated fatty acids. Analysis of the hepatic lipidome demonstrated that TRF did not elevate LCPUFA while reducing steatosis. However, TRF created (1) a separate hepatic lipid signature for triacylglycerols, phosphatidylcholine, and phosphatidylethanolamine species and (2) modified gene and protein expression consistent with reduced fatty acid synthesis and restoration of diurnal gene signaling. TRF increased the saturated fatty acid content in visceral adipose tissue. In summary, TRF of a HF diet alters the lipidomic profile of plasma, liver, and adipose tissue, creating a third distinct lipid metabolic state indicative of positive metabolic adaptations following HF intake.

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Time-restricted feeding mice a high-fat diet induces a unique lipidomic profile

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