Long-term High-fat-diet Feeding Impairs Mitochondrial Biogenesis in Liver of Male and Female Rats

Nadal-Casellas, Antònia; Amengual-Cladera, Emilia; Proenza, Ana M.; Lladó, Isabel; Gianotti, Magdalena

doi:10.1159/000320552

Cited by 61 publications

(41 citation statements)

References 67 publications

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“…Sex differences have been previously described in mitochondrial biogenesis of skeletal muscle [19] and of other tissues, such as liver [20,21] brain [22], heart [23] and brown adipose tissue [24,25]. Moreover, we have also reported a higher skeletal muscle antioxidant capacity and a better insulin sensitivity profile in response to high fat diet (HFD) feeding in female rats compared to males [26].…”

Section: Introductionmentioning

confidence: 54%

Long-term high-fat-diet feeding induces skeletal muscle mitochondrial biogenesis in rats in a sex-dependent and muscle-type specific manner

et al. 2012

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BackgroundMitochondrial dysfunction is thought to play a crucial role in the etiology of insulin resistance, in which skeletal muscle is the main tissue contributor. Sex differences in skeletal muscle insulin and antioxidant responses to high-fat-diet (HFD) feeding have been described. The aim of this study was to elucidate whether there is a sex dimorphism in the effects of HFD feeding on skeletal muscle mitochondrial biogenesis and on the adiponectin signaling pathway, as well as the influence of the muscle type (oxidative or glycolytic).MethodsGastrocnemius and soleus muscles of male and female Wistar rats of 2 months of age fed with a high-fat-diet (HFD) or a low fat diet for 26 weeks were used. Mitochondrial biogenesis and oxidative damage markers, oxidative capacity and antioxidant defences were analyzed. Serum insulin sensitivity parameters and the levels of proteins involved in adiponectin signaling pathway were also determined.ResultsHFD feeding induced mitochondrial biogenesis in both sexes, but to a higher degree in male rats. Although HFD female rats showed greater antioxidant protection and maintained a better insulin sensitivity profile than their male counterparts, both sexes showed an impaired response to adiponectin, which was more evident in gastrocnemius muscle.ConclusionsWe conclude that HFD rats may induce skeletal muscle mitochondrial biogenesis as an attempt to compensate the deleterious consequences of adiponectin and insulin resistance on oxidative metabolism, and that the effects of HFD feeding are sex-dependent and muscle-type specific.

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Section: Introductionmentioning

confidence: 54%

Long-term high-fat-diet feeding induces skeletal muscle mitochondrial biogenesis in rats in a sex-dependent and muscle-type specific manner

et al. 2012

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“…The structural and functional differences of mitochondria between sexes per se may play a role. Male rats show lower mitochondrial oxidative capacity [44] and higher oxidative stress [45] compared to females, which render males more susceptible to diseases associated with mitochondria dysfunction [46]. Early studies have shown that glucocorticoid stimulates mitochondrial RNA synthesis [47], [48], thereby contributes to the regulation of mtDNA encoded OXPHOS gene expression and protein synthesis in mitochondria.…”

Section: Discussionmentioning

confidence: 99%

Maternal Low-Protein Diet Affects Epigenetic Regulation of Hepatic Mitochondrial DNA Transcription in a Sex-Specific Manner in Newborn Piglets Associated with GR Binding to Its Promoter

Jia

Cong

et al. 2013

PLoS ONE

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Mitochondrial oxidative phosphorylation (OXPHOS) plays an important role in energy homeostasis by controlling electron transfer and ATP generation. Maternal malnutrition during pregnancy affects mitochondrial (mt) DNA-encoded OXPHOS activity in offspring, yet it is unknown whether epigenetic mechanism is involved in the transcriptional regulation of mtDNA-encoded OXPHOS genes. In this study, 14 primiparous purebred Meishan sows were fed either standard- (SP, 12% crude protein) or low-protein (LP; 6% crude protein) diets throughout gestation, and the hepatic expression and transcriptional regulation of mtDNA-encoded OXPHOS genes were analyzed in newborn piglets. Maternal low protein diet decreased hepatic mtDNA copy number in males, but not in females. LP male piglets had significantly higher hepatic AMP concentration and low energy charge, which was accompanied by enhanced mRNA expression of NADH dehydrogenase subunits 6, cytochrome c oxidase subunit 1, 2, 3 and cytochrome b, as well as increased cytochrome c oxidase enzyme activity. In contrast, LP female piglets showed significantly lower hepatic AMP concentrations and higher energy charge with no alterations in OXPHOS gene expression. Moreover, LP males demonstrated higher glucocorticoid receptor (GR) binding to the mtDNA promoter compared with SP males, which was accompanied by lower cytosine methylation and hydroxymethylation on mtDNA promoter. Interestingly, opposite changes were seen in females, which showed diminished GR binding and enriched cytosine methylation and hydroxymethylation on mtDNA promoter. These results suggest that maternal low protein diet during pregnancy causes sex-dependent epigenetic alterations in mtDNA-encoded OXPHOS gene expression, possibly GR is involved in mtDNA transcription regulation.

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“…Thus, E2 has a beneficial role in some tissues such as: heart, brain, muscle, brown adipose tissue, and liver [32][33][34], where this hormone increases mitochondrial function. This effect agrees with studies that shown more functional mitochondria in female rats and these findings have been associated with a lower oxidative stress [35,36].…”

Section: Discussionmentioning

confidence: 99%

The Effects of 17β-estradiol on Mitochondrial Biogenesis and Function in Breast Cancer Cell Lines are Dependent on the ERα/ERβ Ratio

Sastre‐Serra

Nadal-Serrano

Pons

et al. 2012

Cell Physiol Biochem

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Background/Aims: 17β-estradiol (E2) is a risk factor for the development of breast cancer, and cause tumorigenesis in epithelial breast cells. Moreover, E2 has distinct effects on different tissues that are attributed to the presence of two estrogen receptor isoforms, ERα and ERβ. Methods: The effect of E2 on mitochondrial biogenesis and function was investigated in two breast cancer cell lines with different estrogen receptor ratios, MCF-7 (high ERα/ERβ ratio) and T47D (low ERα/ERβ ratio) cell lines treated with physiological concentrations of E2 (1 nM). Results: Mitochondria of the MCF-7 cell line showed an increase in proliferation but a decrease in functionality, while the T47D cell line, with low ERα/ERβ ratio, maintained functionality with fewer mitochondria. Conclusion: Our results suggest that ERs endowment and its subtypes relation have an effect on treatment response and could contribute new ideas about mitochondria and ERs in breast cancer, as well as new indicators to the disease progression.

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Long-term High-fat-diet Feeding Impairs Mitochondrial Biogenesis in Liver of Male and Female Rats

Cited by 61 publications

References 67 publications

Long-term high-fat-diet feeding induces skeletal muscle mitochondrial biogenesis in rats in a sex-dependent and muscle-type specific manner

Long-term high-fat-diet feeding induces skeletal muscle mitochondrial biogenesis in rats in a sex-dependent and muscle-type specific manner

Maternal Low-Protein Diet Affects Epigenetic Regulation of Hepatic Mitochondrial DNA Transcription in a Sex-Specific Manner in Newborn Piglets Associated with GR Binding to Its Promoter

The Effects of 17β-estradiol on Mitochondrial Biogenesis and Function in Breast Cancer Cell Lines are Dependent on the ERα/ERβ Ratio

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