Lifestyle intervention and fatty liver disease: The importance of both disrupting inflammation and reducing visceral fat

Malavazos, Alexis Elias; Gobbo, Giulia; Zelaschi, Roberta; Cereda, Emanuele

doi:10.1002/hep.23409

Cited by 4 publications

(3 citation statements)

References 11 publications

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“…Increased lipid uptake by liver as a result of increased fatty acid flow from circulation coming from intra-abdominal fat deposition attributed to the increased food intake after estrogens withdrawal can primarily and partially explain hepatic fat accumulation. The portal/fatty acid flux theory suggests that visceral fat, via its unique location and enhanced lipolytic activity, releases toxic-free fatty acids, which are delivered in high concentrations directly to the liver [ 62 ]. However, the portal/fatty acid flux theory has been questioned with the observation that the bulk of portal vein free fatty acids originate from subcutaneous adipose tissue in overnight-fasted obese individuals [ 63 ].…”

Section: Estrogens Withdrawal In Animals: Central and Peripheral Ementioning

confidence: 99%

NAFLD, Estrogens, and Physical Exercise: The Animal Model

Lavoie

Pighon

2012

Journal of Nutrition and Metabolism

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One segment of the population that is particularly inclined to liver fat accumulation is postmenopausal women. Although nonalcoholic hepatic steatosis is more common in men than in women, after menopause there is a reversal in gender distribution. At the present time, weight loss and exercise are regarded as first line treatments for NAFLD in postmenopausal women, as it is the case for the management of metabolic syndrome. In recent years, there has been substantial evidence coming mostly from the use of the animal model, that indeed estrogens withdrawal is associated with modifications of molecular markers favouring the activity of metabolic pathways ultimately leading to liver fat accumulation. In addition, the use of the animal model has provided physiological and molecular evidence that exercise training provides estrogens-like protective effects on liver fat accumulation and its consequences. The purpose of the present paper is to present information relative to the development of a state of NAFLD resulting from the absence of estrogens and the role of exercise training, emphasizing on the contribution of the animal model on these issues.

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Section: Estrogens Withdrawal In Animals: Central and Peripheral Ementioning

confidence: 99%

NAFLD, Estrogens, and Physical Exercise: The Animal Model

Lavoie

Pighon

2012

Journal of Nutrition and Metabolism

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“…Currently, lifestyle intervention remains a major treatment approach for fatty liver [2,7]. Transient receptor potential vanilloid 1 (TRPV1) is able to sense a plethora of endogenous physical and chemical stimuli and transduce noxious heat and painful stimuli [12][13][14]26].…”

Section: Introductionmentioning

confidence: 99%

TRPV1 activation prevents nonalcoholic fatty liver through UCP2 upregulation in mice

Chen

et al. 2012

Pflugers Arch - Eur J Physiol

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Nonalcoholic fatty liver is characterized by the fatty deformation and lipid deposition of hepatic parenchymal cells that are associated with cardiometabolic diseases. In this study, we report the effect of capsaicin on its receptor, transient receptor potential vanilloid 1 (TRPV1) cation channel, in preventing fatty liver formation. Functional TRPV1 has been detected in hepatocytes and liver tissues. TRPV1 activation by capsaicin reduced lipid accumulation and triglyceride level in the liver from wild-type (WT) mice. However, these effects were absent in the liver from TRPV1(-/-) mice. Chronic dietary capsaicin increased the hepatic uncoupling protein 2 (UCP2) expression in WT but not in TRPV1(-/-) mice (P < 0.01). We conclude that TRPV1 long-time activation might prevent high-fat diet-induced fatty liver in mice through upregulation of hepatic UCP2. Dietary capsaicin may represent a promising intervention in populations at high risk for fatty liver.

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“…[37] Visceral fat, via its unique location and enhanced lipolytic activity, releases toxic-free fatty acids, which are delivered in high concentrations directly to the liver; therefore, excess intraabdominal fat deposition after estrogens withdrawal can primarily and partially explain hepatic fat accumulation. [38] Our results revealed that both caloric restriction and E 2 replacement were equivalent in decreasing liver TAG in comparison with OVX group. In line,…”

Section: Discussionmentioning

confidence: 50%

Modulation of Fetuin-A by Estrogen and Caloric Restriction in Experimental Rat Model of Menopause

Samya

Sokkary

2015

BESPS

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Background and objectives: Menopause is accompanied by higher prevalence of atherogenic lipid profiles, central obesity, and insulin resistance. Hepatic steatosis is frequent in postmenopausal women. Fetuin-A level is strongly related to liver fat content. Its role in menopausal metabolic derangements is largely unknown. We aimed to investigate the relation between fetuin-A and the development of menopausal metabolic complications related to obesity and if caloric restriction/estrogen supplementation could alleviate these abnormalities. Methods: Adult female Wistar rats were either bilaterally ovariectomized (OVX) (30 rats) or sham operated (sham group, n=10 rats). OVX rats were randomly subdivided into ovariectomized group (OVX), ovariectomized group treated with 17-β estradiol (OVX+E 2), and ovariectomized-caloric restricted group (OVX+CR) (n=10/group). Thirteen weeks following surgery, serum levels of glucose, insulin, lipids, fetuin-A and adiponectin were estimated. Weight of visceral fat and triacylglycerol (TAG) content of liver were assessed. Results: Serum fetuin-A level was increased following ovariectomy (113%, P<0.001). This was associated with increased visceral adiposity, abnormal lipid profile, insulin resistance, hypoadiponectinaemia and excessive accumulation of hepatic triacylglycerol (TAG). However, estrogen (E 2) supplementation/caloric restriction (CR) significantly suppressed elevated Fetuin-A (by 41.9%, P<0.001 and 31.2%, P<0.001, respectively). In addition, CR was equally effective as E 2 replacement in reversing metabolic abnormalities. Conclusion: Fetuin-A could be one of the factors contributing to the development of metabolic complications related to menopausal obesity. Caloric restriction alone can ameliorate those complications without the hazardous effects of estrogen replacement; possibly, through inhibition of serum fetuin-A level.

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Lifestyle intervention and fatty liver disease: The importance of both disrupting inflammation and reducing visceral fat

Abstract: hepatocyte-like cells. However, we then used human iPSCs while maintaining higher expressions of p21 than p53 in order to avoid tumorigenicity of the human iPSCs and to increase the value of the cells as research tools.

Cited by 4 publications

References 11 publications

NAFLD, Estrogens, and Physical Exercise: The Animal Model

NAFLD, Estrogens, and Physical Exercise: The Animal Model

TRPV1 activation prevents nonalcoholic fatty liver through UCP2 upregulation in mice

Modulation of Fetuin-A by Estrogen and Caloric Restriction in Experimental Rat Model of Menopause

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