Insulin resistance and steatosis in humans

Capeau, Jacqueline

doi:10.1016/s1262-3636(08)74600-7

Cited by 110 publications

(84 citation statements)

References 38 publications

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“…These findings indicate that rats raised on an SP diet for 14 weeks have already acquired defective insulin signaling. Insulin is a strong activator of the lipogenic pathway through the activation of lipogenic transcription factors such as SREBF1 and ChREBP (Capeau 2008). In this study, we showed that SREBF1 and ChREBP levels in SP rats are markedly increased compared with those in CP rats.…”

Section: Discussionmentioning

confidence: 49%

Possible involvement of food texture in insulin resistance and energy metabolism in male rats

Bae

Hasegawa

Akieda-Asai

et al. 2014

Journal of Endocrinology

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Food texture is known to affect energy metabolism. Although feeding with soft pellets (SP) or via a tube is known to cause increases in body weight, it is unclear how different food textures influence energy metabolism. In this study, we investigated the effects of two different food textures on energy balance and glucose and lipid metabolism in male Wistar rats. The rats were fed SP or control pellets (CP) on a 3-h restricted feeding schedule for 14 weeks and their energy intake, body weight, and energy expenditure were examined. The levels of gastrointestinal hormones, glucose and insulin, were investigated at pre-, mid, and post-feeding. Glucose tolerance and insulin tolerance tests were conducted, and the expressions of molecules involved in the insulin signaling system or lipogenesis in the liver were examined. Histological investigation of pancreatic islets was carried out using anti-insulin and anti-Ki-67 antibodies. Furthermore, the expression in the liver and circulating blood of microRNA-33 (miR-33), which regulates insulin receptor substance 2, was examined. There were no significant differences in energy intake, body weight, or gastrointestinal hormone levels between the SP and CP rats; however, the SP rats showed glucose intolerance and insulin resistance with disruption of insulin signaling. Increases in lipogenic factors and miR-33 expression were also found in the SP rats. The numbers of insulin-positive areas and Ki-67-positive cells of SP rats were significantly increased. This study shows that a soft food texture causes diabetes without obesity, so differences in food texture may be an important factor in type 2 diabetes.

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Section: Discussionmentioning

confidence: 49%

Possible involvement of food texture in insulin resistance and energy metabolism in male rats

Bae

Hasegawa

Akieda-Asai

et al. 2014

Journal of Endocrinology

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“…Recent studies focused on the possible link between psoriasis, obesity and metabolic syndrome, which are known risk factors for NAFLD [44] . It is known that, after the age of 40 years, the psoriatic patients have a higher prevalence of metabolic syndrome and an increased risk for the each components of MetS than controls [11] .…”

Section: Psoriasis and Nafld: Epidemiologymentioning

confidence: 99%

Non-alcoholic fatty liver disease and psoriasis: So far, so near

Ganzetti

Campanati

Offidani

2015

WJH

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Psoriasis is a chronic inflammatory immune-mediated skin diseases which is frequently associated to comorbidities. Non-alcoholic fatty liver disease (NAFLD) is defined as an excessive accumulation of triglycerides in hepatocytes and includes a wide spectrum of liver conditions ranging from relatively benign steatosis to non-alcoholic steatohepatitis with fatty infiltration and lobular inflammation and to cirrhosis and endstage liver disease. Actually, psoriasis is considered a systemic diseases associated to comorbidities, as metabolic syndrome and NAFLD is seen the hepatic manifestation of the metabolic syndrome. The possible link between psoriasis, obesity and metabolic syndrome, which are known risk factors for NAFLD has been recently documented focusing in the crucial role of the adipose tissue in the development of the inflammatory background sharing by the above entities. According to recent data, patients with psoriasis show a greater prevalence of NAFLD and metabolic syndrome than the general population. Moreover, patients with NAFLD and psoriasis are at higher risk of severe liver fibrosis than those with NAFLD and without psoriasis. The link between these pathological conditions appears to be a chronic low-grade inflammatory status. The aim of this review is to focus on the multiple aspects linking NAFLD and psoriasis, only apparently far diseases. Core tip: The review focuses on the multiple physiopathogenetic aspects of the possible link between psoriasis and non-alcoholic fatty liver disease (NAFLD) emphasizing the most recent scientific data. The importance of the multidisciplinary approach to patients affected by psoriasis is underlined and the therapeutic options to treat concomitant psoriasis and NAFLD is discussed evaluating the risk benefit of both biologic and non-biologic therapies.Ganzetti G, Campanati A, Offidani A. Non-alcoholic fatty liver disease and psoriasis: So far, so near. World J Hepatol 2015; 7(3): 315-326 Available from:

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“…These disease states are linked by the presence of hepatic steatosis or steatohepatitis with hepatic insulin resistance, endoplasmic reticulum (ER) stress, and increased generation of cytotoxic sphingolipids, including ceramides (de la Monte, Tong et al 2006;Lester-Coll, Rivera et al 2006;Moroz, Tong et al 2008;Lyn-Cook, Lawton et al 2009;Tong, Neusner et al 2009;Tong, Longato et al 2010). Mechanistically, inflammation, superimposed on disease states that promote lipid storage in hepatocytes, results in progressive ER stress, oxidative damage, mitochondrial dysfunction, and lipid peroxidation, which together promote hepatic insulin resistance (Capeau 2008;Kraegen and Cooney 2008). Hepatic insulin resistance stimulates lipolysis (Kao, Youson et al 1999), and lipolysis leads to increased generation of toxic lipids e.g.…”

Section: Neurotoxic Lipids and Neurodegenerationmentioning

confidence: 99%