A high fat diet with a high C18:0/C16:0 ratio induced worse metabolic and transcriptomic profiles in C57BL/6 mice

Abstract

Background: Differential effects of individual saturated fatty acids (SFAs), particularly stearic acid (C18:0) relative to the shorter-chain SFAs have drawn an interest for more accurate nutritional guidelines. But specific biologic and pathologic functions that can be assigned to particular SFAs are very limited. The present study was designed to compare changes in metabolic and transcriptomic profiles in mice caused by high C18:0 diet and high palmitic acid (C16:0) diet. Methods: Male C57BL/6 mice were assigned to a normal fat diet (NFD), a high fat diet with high C18:0 / C16:0 ratio (HSF) or an isocaloric high fat diet with a low C18:0 / C16:0 ratio (LSF) for 10 weeks. Oral glucose tolerance test, 72h-energy expenditure measurement and CT scan of body fat were done before sacrifice. Fasting glucose and lipids were determined by an auto-biochemical analyzer. Blood insulin, tumor necrosis factor-α (TNF-α)，and interleukin-6 (IL-6) were measured by enzyme linked immunosorbent assay methods. Free fatty acids (FFAs) profiles in blood and liver were determined by using Gas Chromatography-Mass Spectrometry. Microarray analysis was applied to investigate changes in transcriptomic profiles in liver. Pathway analysis and Gene Ontology analysis were applied to describe the roles of differentially expressed mRNAs. Results: Compared with NFD group, body weight, body fat ratio, fasting blood glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), triglyceride, IL-6, serum and liver FFAs including total FFAs, C16:0 and C18:0 were increased in both high fat diet groups, which were much higher in HSF group than those in LSF group. There were much more differentially expressed lncRNAs and mRNAs in HSF mice than those in LSF mice, with distinguishable lncRNA, microRNA, and mRNA expression profiles between these two groups. And some biological functions and pathways, except for energy metabolism regulation, were identified that differentially expressed mRNAs between HSF group and LSF group probably involved in. Conclusion: The high fat diet with a high C18:0/C16:0 ratio induced much severe glucose and lipid metabolic disorders and inflammation, and affected more lncRNAs and mRNAs expression than an isocaloric low C18:0/C16:0 ratio diet in mice.

LPGAT1 controls the stearate/palmitate ratio of phosphatidylethanolamine and phosphatidylcholine in sn-1 specific remodeling

“…The relative abundance of palmitate and stearate seems to be significant. Studies have demonstrated that either the genetic manipulation of the palmitate/stearate ratio in phospholipids (21) or the dietary alteration of the palmitate/stearate ratio (22) affect insulin resistance and body fat ratio. Thus, it seems likely that the palmitate/stearate ratio requires regulation.…”

Nutritional and chemical composition of different life stages of Tribolium castaneum (Herbst)

“…These tendencies were observed in all life stages, probably being a trend in T. castaneum species, when fed on maize flour. The ratio between stearic acid and palmitic acid (C18:0/C16:0) may induce worse lipid profile, insulin resistance, and alter mRNA expression, being advised to be taken into account for evaluating nutritional resources (Wang et al, 2020). In T. castaneum it was observed that this ratio was small, as palmitic acid is more abundant than stearic acid.…”

(Wh)olistic (E)ndocannabinoidome-Microbiome-Axis Modulation through (N)utrition (WHEN) to Curb Obesity and Related Disorders

“…Catabolism of PEA in the body gives rise to relatively inactive products (C16:0 and ethanolamine), causing no adverse effects [52]; therefore, its overall safety and efficacy profile makes it suitable for prophylactic use. However, the overconsumption of C16:0 due to nutritional imbalance and its adverse effects have also been reported in cardiometabolic and liver health [53], aggravating insulin resistance, metabolic dysregulation and dyslipidemia, thereby leading to abnormal fat distribution and deposition [54]. Indeed, a well-balanced dietary approach would be a key to keep a check on DNL.…”