Beneficial Effects of Dietary Fish-Oil-Derived Monounsaturated Fatty Acids on Metabolic Syndrome Risk Factors and Insulin Resistance in Mice

Zhihong, Yang; Miyahara, Hiroko; Mori, Tsuneatsu; Doisaki, Nobushige; Hatanaka, Akimasa

doi:10.1021/jf201496h

Cited by 41 publications

(61 citation statements)

References 37 publications

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“…For example, supplementation of eicosapentaenoate and DHA protects mice from HF-induced body weight gain, dyslipidemia, and glucose intolerance (23). Dietary supplementation with monounsaturated FAs improves insulin sensitivity and adipokine and lipid profiles in the HF-fed mice and healthy young subjects (44,47). Although no evidence directly addresses the relationship between dietary unsaturated FAs and in vivo mitochondrial morphology, our results, together with those of other studies, suggest that supplementation with unsaturated FAs can reverse insulin resistance and in vivo mitochondrial morphology defects.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Fission Contributes to Mitochondrial Dysfunction and Insulin Resistance in Skeletal Muscle

Jheng

Tsai

Guo

et al. 2012

Molecular and Cellular Biology

526

471

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Mitochondrial dysfunction in skeletal muscle has been implicated in the development of insulin resistance and type 2 diabetes. Considering the importance of mitochondrial dynamics in mitochondrial and cellular functions, we hypothesized that obesity and excess energy intake shift the balance of mitochondrial dynamics, further contributing to mitochondrial dysfunction and metabolic deterioration in skeletal muscle. First, we revealed that excess palmitate (PA), but not hyperglycemia, hyperinsulinemia, or elevated tumor necrosis factor alpha, induced mitochondrial fragmentation and increased mitochondrion-associated Drp1 and Fis1 in differentiated C2C12 muscle cells. This fragmentation was associated with increased oxidative stress, mitochondrial depolarization, loss of ATP production, and reduced insulin-stimulated glucose uptake. Both genetic and pharmacological inhibition of Drp1 attenuated PA-induced mitochondrial fragmentation, mitochondrial depolarization, and insulin resistance in C2C12 cells. Furthermore, we found smaller and shorter mitochondria and increased mitochondrial fission machinery in the skeletal muscle of mice with genetic obesity and those with diet-induced obesity. Inhibition of mitochondrial fission improved the muscle insulin signaling and systemic insulin sensitivity of obese mice. Our findings indicated that aberrant mitochondrial fission is causally associated with mitochondrial dysfunction and insulin resistance in skeletal muscle. Thus, disruption of mitochondrial dynamics may underlie the pathogenesis of muscle insulin resistance in obesity and type 2 diabetes.T he prevalence of obesity and type 2 diabetes is increasing at an alarming rate in industrialized countries, partly due to excess food intake and physical inactivity. Excess dietary fat and sugar leads to increased flux of energy fuel substrates and increased lipid burden in peripheral tissues. Skeletal muscle is the major site of glucose uptake and metabolism. Increased fatty acid (FA) uptake contributes to increased lipid accumulation in skeletal muscle, leading to lipotoxicity, which is known to impair muscle insulin sensitivity (2,20). In addition, the intracellular lipid metabolites have been shown to activate serine/threonine protein kinases and suppress insulin actions (37).Mitochondria are important organelles for cellular function through regulation of energy metabolism, ATP generation, and calcium handling. Substantial evidence shows that mitochondrial dysfunction and impairment of the oxidative capacity in skeletal muscle are key mechanisms mediating insulin resistance (24, 34). A reduction in the number and function of mitochondria has been documented in the skeletal muscle of type 2 diabetic patients and animals. For example, the activity of the electron transport chain in subsarcolemmal mitochondria is dramatically reduced in type 2 diabetic and obese subjects, compared with that in lean subjects (36). Furthermore, patients with severe insulin resistance exhibit decreased mitochondrial oxidative activity and ATP s...

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Section: Discussionmentioning

confidence: 99%

Mitochondrial Fission Contributes to Mitochondrial Dysfunction and Insulin Resistance in Skeletal Muscle

Jheng

Tsai

Guo

et al. 2012

Molecular and Cellular Biology

526

471

View full text Add to dashboard Cite

show abstract

“…Recently, Yang and others examined the effect of LC-MUFA-concentrated oil on metabolic disorders and found that consumption of LC-MUFA at a dose of 4-7 w/w improves several metabolic parameters in obese and type 2 diabetic mice 45,46 . Based on these results, there is a possibility that eicosenoic acid plays a role in the positive effect of SO on lipid metabolism.…”

Section: Discussionmentioning

confidence: 99%

Dietary Starfish Oil Prevents Hepatic Steatosis and Hyperlipidemia in C57BL/6N Mice Fed High-fat Diet

Beppu

Yoshinaga

et al. 2017

J. Oleo Sci.

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“…Blood ketone levels remain unchanged after supplementation with fish-oil [42]. Fish-oil supplemented and derived diets in mice reduce total plasma cholesterol and either decrease or have no effect on plasma triglyceride levels [43-45]. Fasting glucose in mice remains unchanged or is decreased in mice given fish-oil supplemented or derived diets [44-46].…”

Section: Introductionmentioning

confidence: 99%

Influence of a ketogenic diet, fish-oil, and calorie restriction on plasma metabolites and lipids in C57BL/6J mice

Meidenbauer

Seyfried

2014

Nutr Metab (Lond)

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BackgroundDiet therapies including calorie restriction, ketogenic diets, and fish-oil supplementation have been used to improve health and to treat a variety of neurological and non-neurological diseases.MethodsWe investigated the effects of three diets on circulating plasma metabolites (glucose and β-hydroxybutyrate), hormones (insulin and adiponectin), and lipids over a 32-day period in C57BL/6J mice. The diets evaluated included a standard rodent diet (SD), a ketogenic diet (KD), and a standard rodent diet supplemented with fish-oil (FO). Each diet was administered in either unrestricted (UR) or restricted (R) amounts to reduce body weight by 20%.ResultsThe KD-UR increased body weight and glucose levels and promoted a hyperlipidemic profile, whereas the FO-UR decreased body weight and glucose levels and promoted a normolipidemic profile, compared to the SD-UR. When administered in restricted amounts, all three diets produced a similar plasma metabolite profile, which included decreased glucose levels and a normolipidemic profile. Linear regression analysis showed that circulating glucose most strongly predicted body weight and triglyceride levels, whereas calorie intake moderately predicted glucose levels and strongly predicted ketone body levels.ConclusionsThese results suggest that biomarkers of health can be improved when diets are consumed in restricted amounts, regardless of macronutrient composition.

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Beneficial Effects of Dietary Fish-Oil-Derived Monounsaturated Fatty Acids on Metabolic Syndrome Risk Factors and Insulin Resistance in Mice

Cited by 41 publications

References 37 publications

Mitochondrial Fission Contributes to Mitochondrial Dysfunction and Insulin Resistance in Skeletal Muscle

Mitochondrial Fission Contributes to Mitochondrial Dysfunction and Insulin Resistance in Skeletal Muscle

Dietary Starfish Oil Prevents Hepatic Steatosis and Hyperlipidemia in C57BL/6N Mice Fed High-fat Diet

Influence of a ketogenic diet, fish-oil, and calorie restriction on plasma metabolites and lipids in C57BL/6J mice

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