Changes in Triacylglycerol‐Accumulated Fiber Type, Fiber Type Composition, and Biogenesis in the Mitochondria of the Soleus Muscle in Obese Rats

Kaneko, Syuhei; Iida, Ryohei; Suga, Takeo; Fukui, Tadayoshi; Morito, Mitsuhiko; Yamane, Akira

doi:10.1002/ar.21472

Cited by 20 publications

(16 citation statements)

References 31 publications

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“…The consumption of a HFD resulted in an increased BMI and muscle mass. In line with previous studies (Andrich et al, 2018;Baek et al, 2018;Eshima et al, 2017;Hegarty et al, 2002;Kaneko et al, 2011;Silvennoinen et al, 2013), this was accompanied by elevated IMCL levels in the soleus, diaphragm and EDL of our mice. This HFD-induced increase in body mass, BMI and IMCL occurred after only 9 weeks in old mice, but was only seen after 16 weeks in the young-adult mice, similar to the absence of changes in IMCL after 4 weeks and elevated IMCL levels after 12 weeks of a HFD seen by others in young-adult mice (Eshima et al, 2017).…”

Section: Effects Of Hfd On Body Mass and Imcl Levelssupporting

confidence: 93%

The impact of a high-fat diet in mice is dependent on duration and age, and differs between muscles

Messa

Piasecki

Hurst

et al. 2020

Journal of Experimental Biology

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Prolonged high-fat diets (HFDs) can cause intramyocellular lipid (IMCL) accumulation that may negatively affect muscle function. We investigated the duration of a HFD required to instigate these changes, and whether the effects are muscle specific and aggravated in older age. Muscle morphology was determined in the soleus, extensor digitorum longus (EDL) and diaphragm muscles of female CD-1 mice from 5 groups: young fed a HFD for 8 weeks (YS-HFD, n=16), young fed a HFD for 16 weeks (YL-HFD, n=28) and young control (Y-Con, n=28). The young animals were 20 weeks old at the end of the experiment. Old (70 weeks) female CD-1 mice received either a normal diet (O-Con, n=30) or a HFD for 9 weeks (OS-HFD, n=30). Body mass, body mass index and intramyocellular lipid (IMCL) content increased in OS-HFD (P≤0.003). In the young mice, this increase was seen in YL-HFD and not YS-HFD (P≤0.006). The soleus and diaphragm fibre cross-sectional area (FCSA) in YL-HFD was larger than that in Y-Con (P≤0.004) while OS-HFD had a larger soleus FCSA compared with that of O-Con after only 9 weeks on a HFD (P<0.001). The FCSA of the EDL muscle did not differ significantly between groups. The oxidative capacity of fibres increased in young mice only, irrespective of HFD duration (P<0.001). High-fat diet-induced morphological changes occurred earlier in the old animals than in the young, and adaptations to HFD were muscle specific, with the EDL being least responsive.

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Section: Effects Of Hfd On Body Mass and Imcl Levelssupporting

confidence: 93%

The impact of a high-fat diet in mice is dependent on duration and age, and differs between muscles

Messa

Piasecki

Hurst

et al. 2020

Journal of Experimental Biology

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“…We have shown previously that mitochondrial protein synthesis was specifically affected during obesity (Guillet et al 2009). Muscle mitochondrial alterations were often reported during obesity in association with lipid infiltration (Kaneko et al 2011). It is not surprising therefore that the protein fraction primarily affected in this situation is the mitochondrial protein fraction.…”

Section: Discussionmentioning

confidence: 99%

Time‐course changes of muscle protein synthesis associated with obesity‐induced lipotoxicity

Masgrau

Mishellany-Dutour

Murakami

et al. 2012

The Journal of Physiology

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Key points• Prolonged obesity leads to ectopic lipid accumulation in non-adipose tissues, particularly in skeletal muscles, inducing metabolic dysfunctions (reduced glucose uptake, mitochondria dysfunction, lipotoxicity).• Several studies in humans and rodents have shown that obesity induces a short-term increase in fat-free mass but a long-term decrease in skeletal muscle mass.• We investigated the mechanisms potentially involved in muscle loss by measuring simultaneously protein synthesis and lipid infiltration in different types of skeletal muscles, during the development of obesity.• Our results show that protein synthesis rate in glycolytic muscles increased together with muscle mass during the early phase of obesity development, whereas it decreased later. Reduced protein synthesis rate was associated with a high lipid accumulation in glycolytic muscles.• These results suggest that lipid accumulation in muscles during prolonged obesity is deleterious for amino acid incorporation in skeletal muscle proteins, and thus indirectly for muscle mass.Abstract The object of the study was to investigate the sequential changes of protein synthesis in skeletal muscle during establishment of obesity, considering muscle typology. Adult Wistar rats were fed a standard diet for 16 weeks (C; n = 14), or a high-fat, high-sucrose diet for 16 (HF16; n = 14) or 24 weeks (HF24; n = 15). Body composition was measured using a dual-energy X-ray absorptiometry scanner. The fractional synthesis rates (FSRs) of muscle protein fractions were calculated in tibialis anterior (TA) and soleus muscles by incorporation of L-13 C-valine in muscle protein. Muscle lipid and mitochondria contents were determined using histochemical analysis. Obesity occurred in an initial phase, from 1 to 16 weeks, with an increase in weight (P < 0.05), fat mass (P < 0.001), muscle mass (P < 0.001) and FSR in TA (actin: 5.3 ± 0.2 vs. 8.8 ± 0.5% day −1 , C vs. HF16, P < 0.001) compared with standard diet. The second phase, from 16 to 24 weeks, was associated with a weight stabilization, a decrease in muscle mass (P < 0.05) and a decrease in FSR in TA (mitochondrial: 5.6 ± 0.2 vs. 4.2 ± 0.4% day −1 , HF16 vs. HF24, P < 0.01) compared with HF16 group. Muscle lipid content was increased in TA in the second phase of obesity development (P < 0.001). Muscle mass, lipid infiltration and muscle protein synthesis were differently affected, depending on the stage of obesity development and muscle typology. Chronic lipid infiltration in glycolytic muscle is concomitant with a reduction of muscle protein synthesis, suggesting that muscle lipid infiltration in response to a high-fat diet is deleterious for the incorporation of amino acid in skeletal muscle proteins.

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“…Both types of lipid can weaken muscle contractility; accordingly, their accumulation in urethral striated muscle may result in sphincter dysfunction. IMCLs could also lead to the suppression of biogenesis, inhibition of mitochondrial function and alteration in the fibre type composition of the obese rat . To validate the hypothesis, therefore, that urethral dysfunction is a contributor to obesity‐associated SUI, the present study aimed to elucidate how obesity affects the structure and function of the female urethral sphincter in a rat model of genetic obesity.…”

Section: Introductionmentioning

confidence: 95%

Transgenic animal model for studying the mechanism of obesity‐associated stress urinary incontinence

et al. 2016

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Purpose To study and compare the function and structure of the urethral sphincter in female Zucker lean and Zucker fatty (ZF) rats and to assess viability of ZF fats as a model for female obesity-associated stress urinary incontinence (OA-SUI). Materials and Methods Twelve16-week-old female Zucker Lean (ZUC-Leprfa 186) (ZL) rats and twelve16-week-old female Zucker Fatty (ZUC-Leprfa 185) (ZF) rats were grouped into two groups: ZL arm and ZF arm. Intraperitoneal insulin tolerance testing was carried out before functional study. Metabolic cages, conscious cystometry, and leak point pressure (LPP) were conducted. Urethral tissues were harvested for immunofluorescence staining to check intramyocellular lipid (IMCL) and sphincter muscle (smooth muscle and striated muscle) composition. Results The ZF rats demonstrated insulin resistance, increased voiding frequency, and decreased LPP compared to ZL rats (p<0.05) with more IMCL deposition localized in urethral striated muscle fibers of the ZF rats (p<0.05). The thickness of the striated muscle layer and the ratio of striated muscle to smooth muscle were lower in ZF rats compared to ZL rats. Conclusion Obesity impairs urethral sphincter function by IMCL deposition and leads to atrophy and distortion of urethral striated muscle. The ZF rats could be a consistent and reliable animal model to study obesity-associated stress urinary incontinence (OA-SUI).

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Changes in Triacylglycerol‐Accumulated Fiber Type, Fiber Type Composition, and Biogenesis in the Mitochondria of the Soleus Muscle in Obese Rats

Cited by 20 publications

References 31 publications

The impact of a high-fat diet in mice is dependent on duration and age, and differs between muscles

The impact of a high-fat diet in mice is dependent on duration and age, and differs between muscles

Time‐course changes of muscle protein synthesis associated with obesity‐induced lipotoxicity

Transgenic animal model for studying the mechanism of obesity‐associated stress urinary incontinence

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