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. 2023 Nov 13;15(22):4761.
doi: 10.3390/nu15224761.

Reducing Dietary Polyunsaturated to Saturated Fatty Acids Ratio Improves Lipid and Glucose Metabolism in Obese Zucker Rats

Gianfranca Carta  1 , Elisabetta Murru  1 , Giovanna Trinchese  2 , Gina Cavaliere  3 , Claudia Manca  1 , Maria Pina Mollica  2 , Sebastiano Banni  1
Affiliations

Reducing Dietary Polyunsaturated to Saturated Fatty Acids Ratio Improves Lipid and Glucose Metabolism in Obese Zucker Rats

Gianfranca Carta et al. Nutrients. .

Abstract

We investigated the influence of varying dietary polyunsaturated fatty acid (PUFA)/saturated fatty acids (SFA) ratios on insulin resistance (IR), fatty acid metabolism, N-acylethanolamine (NAE) bioactive metabolite levels, and mitochondrial function in lean and obese Zucker rats in a model designed to study obesity and IR from overnutrition. We provided diets with 7% fat (w/w), with either a low PUFA/SFA ratio of 0.48, predominantly comprising palmitic acid (PA), (diet-PA), or the standard AIN-93G diet with a high PUFA/SFA ratio of 3.66 (control, diet-C) over eight weeks. In obese rats on diet-PA versus diet-C, there were reductions in plasma triglycerides, cholesterol, glucose, insulin concentrations and improved muscle mitochondrial function, inflammatory markers and increased muscle N-oleoylethanolamine (OEA), a bioactive lipid that modulates lipid metabolism and metabolic flexibility. Elevated palmitic acid levels were found exclusively in obese rats, regardless of their diet, implying an endogenous production through de novo lipogenesis rather than from a dietary origin. In conclusion, a reduced dietary PUFA/SFA ratio positively influenced glucose and lipid metabolism without affecting long-term PA tissue concentrations. This likely occurs due to an increase in OEA biosynthesis, improving metabolic flexibility in obese rats. Our results hint at a pivotal role for balanced dietary PA in countering the effects of overnutrition-induced obesity.

Keywords: N-oleoylethanolamine (OEA); dietary fat; fatty acid metabolism; insulin resistance; mitochondria; obesity.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Food intake and growth parameters of lean rats fed diet-C (Lean-C) or diet-PA (Lean-PA), and obese rats fed diet-C (Ob-C) or diet-PA (Ob-PA). Food intake (A); weight gain at 4 weeks (B); and at 8 weeks (C); body length at t0 (D), and at 8 weeks (E); tail length at t0 (F), and at 8 weeks (G); BMI at t0 (H), at 4 weeks (I); and at 8 weeks (J); liver weight (K); BMI/Food Intake at t0 (L), at 4 weeks (M), and at 8 weeks (N); and visceral adipose tissue (VAT) weight (O). Control diet (diet-C); 16:0-enriched diet (diet-PA). Error bars represent SEM (n = 6) * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.
Figure 2
Figure 2
Comparison of total lipids per g of tissue: (A) in liver; and (B) in muscle, in lean rats fed diet-C (Lean-C) or diet-PA (Lean-PA), and obese rats fed diet-C (Ob-C) or diet-PA (Ob-PA). Values are expressed as % of values of Lean-C rats. Control diet (diet-C); 16:0-enriched diet (diet-PA). Error bars represent SEM (n = 6) * p < 0.05; ** p < 0.01; *** p < 0.001.
Figure 3
Figure 3
Liver and muscle levels of N-acylethanolamine (NAE) and 2-arachidonoylglycerol (2-AG). N-palmitoylethanolamine (PEA) (A in liver and F in muscle, respectively); N-palmitoleoylethanolamide (POEA) (B,G); N-oleoylethanolamine (OEA) (C,H); 2-AG (D,I); and OEA/2-AG ratio (E,J), expressed as % of values of lean rats fed diet-C (Lean-C), in lean rats fed diet-PA (Lean-PA), and obese rats fed diet-C (Ob-C) or diet-PA (Ob-PA). Control diet (diet-C); 16:0-enriched diet (diet-PA). Statistical significance among groups was assessed by one-way ANOVA followed by Tukey’s correction for multiple comparisons. Error bars represent SEM (n = 6) * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.
Figure 4
Figure 4
Adipose tissue and plasma levels of N-acylethanolamine (NAE) and 2-arachidonoylglycerol (2-AG). N-palmitoylethanolamine (PEA):(A in adipose tissue and F in plasma. respectively), N-palmitoleoylethanolamide (POEA) (B,G); N-oleoylethanolamine (OEA) (C,H); 2-AG (D,I); and OEA/2-AG ratio (E,J), expressed as % of values of lean rats fed diet-C (Lean-C), in lean rats fed diet-PA (Lean-PA), and obese rats fed diet-C (Ob-C) or diet-PA (Ob-PA). Control diet (diet-C); 16:0-enriched diet (diet-PA). Statistical significance among groups was assessed by one-way ANOVA followed by Tukey’s correction for multiple comparisons. Error bars represent SEM (n = 6) * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.
Figure 5
Figure 5
Plasma, hepatic, and inflammatory parameters: (A) triglycerides (TG); (B) cholesterol; (C) glucose; (D) insulin; (E) homeostasis model assessment-estimated insulin resistance (HOMA-IR); (F) Monocyte chemoattractant protein-1 (MCP1); (G) Alanine transaminase (ALT); (H) aspartate aminotransferase (AST); and (I) TNFα, (J) Interleukin-1 (IL-1)β, measured in lean rats fed diet-C (Lean-C) or diet-PA (Lean-PA), and obese rats fed diet-C (Ob-C) or diet-PA (Ob-PA). Control diet (diet-C); 16:0-enriched diet (diet-PA). Statistical significance among groups was assessed by one-way ANOVA followed by Tukey’s correction for multiple comparisons. Error bars represent SEM (n = 6) * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.
Figure 6
Figure 6
Hepatic mitochondrial respiration. The presence of succinate and rotenone (A); or palmitoyl-carnitine and malate (B) as substrates was determined in presence (state 3) or absence (state 4) of adenosine diphosphate (ADP). Hydrogen peroxide (H2O2) release (C); and superoxide dismutase (SOD) activity (D) were determined in hepatic-isolated mitochondria. Control diet (diet-C); 16:0-enriched diet (diet-PA). Statistical significance among groups was assessed by one-way ANOVA followed by Tukey’s correction for multiple comparisons. Error bars represent SEM (n = 6) * p < 0.05; ** p < 0.01 *** p < 0.001, **** p < 0.0001.
Figure 7
Figure 7
Skeletal muscle mitochondrial respiration. The presence of succinate and rotenone (A); or palmitoyl-carnitine and malate (B) as substrates was determined in the presence (state 3) or absence (state 4) of adenosine diphosphate (ADP). Hydrogen peroxide (H2O2) release (C); and superoxide dismutase (SOD) activity (D) were determined in skeletal-muscle-isolated mitochondria. Control diet (diet-C); 16:0-enriched diet (diet-PA). Statistical significance among groups was assessed by one-way ANOVA followed by Tukey’s correction for multiple comparisons. Error bars represent SEM (n = 6). ** p < 0.01 *** p < 0.001, **** p < 0.0001.
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