Attenuation of obesity and insulin resistance by fish oil supplementation is associated with improved skeletal muscle mitochondrial function in mice fed a high-fat diet

Martins, Amanda Roque; Crisma, Amanda Rabello; Masi, Laureane Nunes; Amaral, Cátia Lira do; Marzuca‐Nassr, Gabriel Nasri; Bomfim, Lucas Henrique Montes; Teodoro, Bruno Gonzaga; Queiroz, André Lima; Serdan, Tamires Duarte Afonso; Torres, Rosângela Pavan; Mancini‐Filho, Jorge; Rodrigues, Alice Cristina; Alba-Loureiro, Tatiana Carolina; Pithon-Curi, Tânia Cristina; Gorjão, Renata; Silveira, Leonardo R.; Curi, Rui; Newsholme, Philip; Hirabara, Sandro Massao

doi:10.1016/j.jnutbio.2017.11.012

Cited by 68 publications

(64 citation statements)

References 102 publications

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“…This report [ 173 ] also shows that intake of omega-3 polyunsaturated fatty acids enhances the insulin signals, Akt and GSK3-beta, indicating that intake of omega-3 polyunsaturated fatty acids improves the high-fat diet-induced insulin resistance. This report [ 173 ] concludes that the action of omega-3 polyunsaturated fatty acids on insulin resistance and levels of blood glucose and insulin is mediated via improvement of skeletal muscle mitochondrial function. However, it is possible that this action of omega-3 polyunsaturated fatty acids [ 173 ] appears via elevation of interstitial fluid pH ( Figure 5 ).…”

Section: Roles Of Foods Containing Weak Organic Acids and Carboxylmentioning

confidence: 81%

“…Namely, the absorbed R-COO − behaves as a ‘base’. A report [ 173 ] indicates that intake of omega-3 polyunsaturated fatty acids (weak organic acids) improves (decreases) high-fat diet-induced high blood glucose, glucose uptake, glucose oxidation and glycogen synthesis. This report [ 173 ] also shows that intake of omega-3 polyunsaturated fatty acids enhances the insulin signals, Akt and GSK3-beta, indicating that intake of omega-3 polyunsaturated fatty acids improves the high-fat diet-induced insulin resistance.…”

Section: Roles Of Foods Containing Weak Organic Acids and Carboxylmentioning

confidence: 99%

“…A report [ 173 ] indicates that intake of omega-3 polyunsaturated fatty acids (weak organic acids) improves (decreases) high-fat diet-induced high blood glucose, glucose uptake, glucose oxidation and glycogen synthesis. This report [ 173 ] also shows that intake of omega-3 polyunsaturated fatty acids enhances the insulin signals, Akt and GSK3-beta, indicating that intake of omega-3 polyunsaturated fatty acids improves the high-fat diet-induced insulin resistance. This report [ 173 ] concludes that the action of omega-3 polyunsaturated fatty acids on insulin resistance and levels of blood glucose and insulin is mediated via improvement of skeletal muscle mitochondrial function.…”

Section: Roles Of Foods Containing Weak Organic Acids and Carboxylmentioning

confidence: 99%

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The Proposal of Molecular Mechanisms of Weak Organic Acids Intake-Induced Improvement of Insulin Resistance in Diabetes Mellitus via Elevation of Interstitial Fluid pH

Marunaka

2018

IJMS

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Blood contains powerful pH-buffering molecules such as hemoglobin (Hb) and albumin, while interstitial fluids have little pH-buffering molecules. Thus, even under metabolic disorder conditions except severe cases, arterial blood pH is kept constant within the normal range (7.35~7.45), but the interstitial fluid pH under metabolic disorder conditions becomes lower than the normal level. Insulin resistance is one of the most important key factors in pathogenesis of diabetes mellitus, nevertheless the molecular mechanism of insulin resistance occurrence is still unclear. Our studies indicate that lowered interstitial fluid pH occurs in diabetes mellitus, causing insulin resistance via reduction of the binding affinity of insulin to its receptor. Therefore, the key point for improvement of insulin resistance occurring in diabetes mellitus is development of methods or techniques elevating the lowered interstitial fluid pH. Intake of weak organic acids is found to improve the insulin resistance by elevating the lowered interstitial fluid pH in diabetes mellitus. One of the molecular mechanisms of the pH elevation is that: (1) the carboxyl group (R-COO−) but not H+ composing weak organic acids in foods is absorbed into the body, and (2) the absorbed the carboxyl group (R-COO−) behaves as a pH buffer material, elevating the interstitial fluid pH. On the other hand, high salt intake has been suggested to cause diabetes mellitus; however, the molecular mechanism is unclear. A possible mechanism of high salt intake-caused diabetes mellitus is proposed from a viewpoint of regulation of the interstitial fluid pH: high salt intake lowers the interstitial fluid pH via high production of H+ associated with ATP synthesis required for the Na+,K+-ATPase to extrude the high leveled intracellular Na+ caused by high salt intake. This review article introduces the molecular mechanism causing the lowered interstitial fluid pH and insulin resistance in diabetes mellitus, the improvement of insulin resistance via intake of weak organic acid-containing foods, and a proposal mechanism of high salt intake-caused diabetes mellitus.

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Section: Roles Of Foods Containing Weak Organic Acids and Carboxylmentioning

confidence: 81%

Section: Roles Of Foods Containing Weak Organic Acids and Carboxylmentioning

confidence: 99%

Section: Roles Of Foods Containing Weak Organic Acids and Carboxylmentioning

confidence: 99%

See 1 more Smart Citation

The Proposal of Molecular Mechanisms of Weak Organic Acids Intake-Induced Improvement of Insulin Resistance in Diabetes Mellitus via Elevation of Interstitial Fluid pH

Marunaka

2018

IJMS

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“…18 The results of the current study demonstrated decreased expression of PGC-1α accompanied with increased expression of FoxO3, atrogin-1/MAFbx, and MuRF-1 in soleus muscle of HFD-fed animals. Martins et al 45 reported that HFD promoted downregulation of PGC-1a expression; this impacted mitochondrial function, biogenesis, and oxidative capacity in skeletal muscle. PGC-1α downregulation in soleus muscle was suggested to be responsible for activating the catabolic systems via FoxO3 disinhibition and the subsequent enhancement of ubiquitin ligase.…”

Section: Discussionmentioning

confidence: 99%

“…14 Overexpression of FoxO3 is known to induce muscle fiber atrophy in vivo 44 ; that is associated with upregulation of MAFbx/atrogin-1 and MuRF-1. Martins et al 45 reported that HFD promoted downregulation of PGC-1a expression; this impacted mitochondrial function, biogenesis, and oxidative capacity in skeletal F I G U R E 5 Immunohistochemical detection of MHC type IIa of (A) control group, (B) HFD-fed rat group, and (C) metformin-treated group (×400, scale bar = 2 0 μm). Martins et al 45 reported that HFD promoted downregulation of PGC-1a expression; this impacted mitochondrial function, biogenesis, and oxidative capacity in skeletal F I G U R E 5 Immunohistochemical detection of MHC type IIa of (A) control group, (B) HFD-fed rat group, and (C) metformin-treated group (×400, scale bar = 2 0 μm).…”

Section: Discussionmentioning

confidence: 99%

Beneficial effects of metformin on muscle atrophy induced by obesity in rats

Hasan

Shalaby

El‐Gendy

et al. 2018

J of Cellular Biochemistry

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Aim A growing interest to understand the signaling pathways mediating obesity‐induced muscle atrophy is given. Metformin (Met) was reported to possess positive effects on preventing muscle damage and promoting muscle mass maintenance. The aim of the present study to investigate pathways involved in Met effect on obesity induced muscle atrophy. Methods Thirty adult male albino rats were assigned into two groups: normal chew diet fed group as control group (C; n = 10) and high‐fat‐diet (HFD) fed group ( n = 20). After 16 weeks, the HFD‐fed animals were subdivided into two groups; HFD group ( n = 10) and HFD fed treated with oral Met (320 mg/day) treatment (Met, n = 10) for 4 weeks. At the end of the experiment; final body weight, visceral fat weight, fasting blood glucose, insulin, lactate, total cholesterol, triglycerides were measured and calculated homeostatic model assessment insulin resistant (HOMA‐IR) for all groups. Soleus muscle weight, histopathlogical examination and expression of peroxisome proliferator‐activated receptor‐γ coactivator‐1α (PGC‐1α), forkhead box O3 (FoxO3), atrogin‐1/MAFbx, and muscle RING finger 1 (MuRF‐1) were performed. Results HFD‐fed animals showed significant increase in final body weight, visceral fat mass, fasting blood glucose, insulin, calculated HOMA‐IR, lactate, total cholesterol and triglycerides with significant decrease in soleus muscle weight, PGC‐1α and significant increase in FoxO3, atrogin‐1/MAFbx, and MuRF‐1 expression. Also, there was significant decrease in fiber diameter, myosin heavy chain (MHC) I content while collagen content and myosin heavy chain IIa were increased compared with control group. Met‐treated group showed a significant decrease in the measured parameters compared with the HFD group. It also restored the gene expression, morphometric measures and MHC composition toward normal. Conclusion The current study is the first to provide evidence that Met could ameliorate muscle atrophy in high‐fat diet induced obesity and this effect may be in part due to regulation of PGC‐1α‐FoxO3 pathway.

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Eicosapentaenoic and Docosahexaenoic Acids Differentially Alter Gut Microbiome and Reverse High‐Fat Diet–Induced Insulin Resistance

Zhuang

Zhang

Shou

et al. 2020

Molecular Nutrition Food Res

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Scope: To assess the individual effects of dietary eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on insulin resistance (IR), gut microbiome, and gut metabolites in high-fat-diet-induced obese (DIO) mice. Methods and results: DIO mice are fed an either high-fat diet (HFD), EPA (1% w/w) enriched HFD, or DHA (1% wt/wt) enriched HFD for 15 weeks. Both EPA and DHA supplements reverse hyperglycemia and IR but do not affect body weight in DIO mice while DHA exhibits a more pronounced ameliorative effect in male mice. Both EPA-and DHA-enriched Lactobacillus and short-chain fatty acids (SCFAs)-producing species from Lachnospiraceae while reduced lipopolysaccharide (LPS)-producing Bilophila and Escherichia/Shigella. Compared with EPA, DHA-supplemented mice have more abundant propionic/butyric acid-producing bacteria, including Coprococcus, Butyricimonas synergistica, Bacteroides acidifaciens, and Intestinimonas, and less-abundant LPS-correlated species Streptococcus and p-75-a5.

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Attenuation of obesity and insulin resistance by fish oil supplementation is associated with improved skeletal muscle mitochondrial function in mice fed a high-fat diet

Cited by 68 publications

References 102 publications

The Proposal of Molecular Mechanisms of Weak Organic Acids Intake-Induced Improvement of Insulin Resistance in Diabetes Mellitus via Elevation of Interstitial Fluid pH

The Proposal of Molecular Mechanisms of Weak Organic Acids Intake-Induced Improvement of Insulin Resistance in Diabetes Mellitus via Elevation of Interstitial Fluid pH

Beneficial effects of metformin on muscle atrophy induced by obesity in rats

Eicosapentaenoic and Docosahexaenoic Acids Differentially Alter Gut Microbiome and Reverse High‐Fat Diet–Induced Insulin Resistance

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