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. 2023 Apr 5;13(1):5556.
doi: 10.1038/s41598-023-32851-7.

Polyunsaturated fatty acids-rich dietary lipid prevents high fat diet-induced obesity in mice

Yuri Haneishi #  1 , Yuma Furuya #  1 , Mayu Hasegawa  1 , Hitoshi Takemae  2 , Yuri Tanioka  3 , Tetsuya Mizutani  2 , Mauro Rossi  4 , Junki Miyamoto  5
Affiliations

Polyunsaturated fatty acids-rich dietary lipid prevents high fat diet-induced obesity in mice

Yuri Haneishi et al. Sci Rep. .

Abstract

Diet is the primary factor affecting host nutrition and metabolism, with excess food intake, especially high-calorie diets, such as high-fat and high-sugar diets, causing an increased risk of obesity and related disorders. Obesity alters the gut microbial composition and reduces microbial diversity and causes changes in specific bacterial taxa. Dietary lipids can alter the gut microbial composition in obese mice. However, the regulation of gut microbiota and host energy homeostasis by different polyunsaturated fatty acids (PUFAs) in dietary lipids remains unknown. Here, we demonstrated that different PUFAs in dietary lipids improved host metabolism in high-fat diet (HFD)-induced obesity in mice. The intake of the different PUFA-enriched dietary lipids improved metabolism in HFD-induced obesity by regulating glucose tolerance and inhibiting colonic inflammation. Moreover, the gut microbial compositions were different among HFD and modified PUFA-enriched HFD-fed mice. Thus, we have identified a new mechanism underlying the function of different PUFAs in dietary lipids in regulating host energy homeostasis in obese conditions. Our findings shed light on the prevention and treatment of metabolic disorders by targeting the gut microbiota.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Figure 1
Figure 1
Acute administration of PUFAs improved glucose metabolism by promoting GLP-1 secretion. (a) GLP-1 secretion in the STC-1 cells treated with each LCFA (n = 6 per group). **P < 0.01; *P < 0.05, vs. Control (Dunn’s test). (b) Experimental scheme. (c) Each mouse was administered LCFAs by oral gavage. After 2 h, the plasma GLP-1 levels were measured (n = 8 mice for each group). **P < 0.01; *P < 0.05, vs Control (Dunn’s test). (d) Each mouse was administered LCFAs by oral gavage. ipGTT was evaluated (left panel) and area under the curve (AUC) of ipGTT was calculated (right panel) after 2 h (n = 7–8 mice for each group). **P < 0.01; *P < 0.05, vs. Control (Dunn’s test for 0, 15, and 30 min and Dunnett test for 60, 90, 120 min, and AUC). Results are presented as means ± standard error.
Figure 2
Figure 2
Polyunsaturated fatty acid-containing dietary lipids prevent high fat diet-induced obesity. (a–d) C57BL/6J male mice were fed either normal chow (NC), a high fat diet (HFD), or a modified HFD diet [Soybean oil in HFD was replaced with either linseed oil (Linseed), fish oil (Fish), or olive oil (Olive)] for 8 weeks. (a) Changes in body and tissue weights. epi epididymal, peri perirenal, sub subcutaneous, WAT white adipose tissue. **P < 0.01; *P < 0.05, vs, NC. ##P < 0.01; #P < 0.05, vs, HFD (Dunn’s test for 8, 15, and 16 weeks of age, and tissue weight and Tukey–Kramer test for 9–14 weeks of age). (b) ipGTT was evaluated at 15 weeks of age. **P < 0.01; *P < 0.05, vs, NC. ##P < 0.01, vs, HFD (Dunn’s test for 0, 30, 90, and 120 min and Tukey–Kramer test for 15 and 60 min). (c,d) After 5 h fasting, blood glucose, plasma triglycerides, non-esterified fatty acids, total cholesterol, GLP-1, insulin, and PYY levels were measured at the end of the experimental period (n = 7–10 mice for each group). **P < 0.01; *P < 0.05 (Dunn’s test for blood glucose, plasma triglycerides, NEFAs, total cholesterol, GLP-1, and insulin and Tukey–Kramer test for PYY). Results are presented as means ± standard error.
Figure 3
Figure 3
Fish oil suppressed WAT inflammation by enhancing intestinal barrier function. (a–d) C57BL/6J male mice were fed either normal chow (NC), a high fat diet (HFD), or a modified HFD diet (Soybean oil in HFD was replaced with either linseed oil (Linseed), fish oil (Fish), or olive oil (Olive)) for 8 weeks. (a) Hematoxylin–eosin (H&E)–stained epididymal WAT and the mean area of adipocytes (n = 4 mice for each group). Scale bar; 400 μm. The mRNA expression of Pparg and Fabp4 in the epididymal WAT (n = 8 mice for each group). **P < 0.01; *P < 0.05 (Tukey–Kramer test for adipocytes size and Fabp4, and Dunn’s test for Pparg). (b) The mRNA expression of Tnfα, F4/80, and Mcp-1 in the epididymal WAT (n = 8 mice for each group). **P < 0.01; *P < 0.05 (Dunn’s test). (c) The mRNA expression of Tnfα in the colon (left panel) and plasma LPS levels (right panel) were measured at the end of the experimental period (n = 7–10 mice for each group). **P < 0.01; *P < 0.05 (Tukey–Kramer test for plasma LPS and Dunn’s test for Tnfα). (d) The mRNA expression of Ocln, and Gcg in the colon (n = 7–8 mice for each group). **P < 0.01; *P < 0.05 (Tukey–Kramer test for Ocln and Dunn’s test for Gcg). Results are presented as means ± standard error.
Figure 4
Figure 4
Fish oil altered the gut microbiota composition. (a–d) C57BL/6J male mice were fed either a high fat diet (HFD) or a modified HFD diet (Soybean oil in HFD was replaced with fish oil (Fish)) for 8 weeks. Gut microbial composition was evaluated for the determination of the relative abundance of microbial phyla (a), Firmicutes to Bacteroidota ratio (b), Chao1 and Shannon index at the OTU level (c), and principal coordinate analysis (PCoA) at the phylum level (d) of mice fed HFD or a modified HFD (Fish) in feces (n = 7–8 mice for each group). *P < 0.05 (Mann–Whitney test).
Figure 5
Figure 5
Fish oil improved metabolic conditions were attenuated in antibiotic-treated mice. (a–e) C57BL/6J male mice were fed either a high fat diet (HFD) or a modified HFD diet (Soybean oil in HFD was replaced with fish oil (Fish)) and treated with antibiotics (Abx.) for 8 weeks. (a) Changes in body and tissue weights. epi epididymal, peri perirenal, sub subcutaneous, WAT white adipose tissue. (b) ipGTT was evaluated at 15 weeks of age. (c,d) After 5 h fasting, blood glucose, plasma triglycerides, non-esterified fatty acids, total cholesterol, GLP-1, insulin, and PYY levels were measured at the end of the experimental period. (e) The mRNA expression of Tnfα and Ocln in the colon (upper panel) and plasma LPS levels (lower panel) were measured at the end of the experimental period (n = 7–9 mice for each group). Results are presented as means ± standard error. NS not significant.
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