Time course of the development of non-alcoholic hepatic steatosis in response to high-fat diet-induced obesity in rats

Gauthier, Marie‐Soleil; Favier, R.; Lavoie, Jean‐Marc

doi:10.1079/bjn20051635

Cited by 104 publications

(89 citation statements)

References 31 publications

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“…Our experimental groups presented relative enlargement of their liver (table 2), reflecting an early sign of the adverse effects of diets rich in saturated fatty acids [35]. Recent studies indicate that increased levels of triglyceride in the liver (steatosis) have also been observed in the adult offspring of dams fed a HF diet, which is in agreement with our findings [36].…”

Section: Discussionsupporting

confidence: 82%

Maternal High-Fat Diet Programs for Metabolic Disturbances in Offspring despite Leptin Sensitivity

et al. 2012

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A fatty diet during pregnancy in mouse dams causes metabolic abnormalities (similar to metabolic syndrome in humans) in the rodents’ offspring. We tested the hypothesis that the offspring of dams fed a high-fat diet during pregnancy and lactation develop metabolic abnormalities and leptin resistance. Pregnant C57BL/6 mice (n = 20) were fed either standard chow (SC; 19% fat) or a high-fat diet (HF; 49% fat). After weaning, male offspring were divided into four groups, according to the diet of dams and offspring: SC(dams)/SC(offspring), SC/HF, HF/SC and HF/HF (n = 30/group). For a metabolic analysis, we evaluated body mass, fat mass depots, blood plasma and adipocyte structure at 12 weeks of age. To analyse leptin sensitivity, each group was divided into two groups (vehicle or leptin) to identify the feeding response and pSTAT3 expression after acute intracerebroventricular (ICV) treatment. The offspring of mothers fed a high-fat diet presented increased body mass and visceral fat, adipocyte hypertrophy and insulin resistance. This phenotype was not associated with central leptin resistance. Thus, maternal programming by HF predisposes offspring to metabolic abnormalities despite leptin sensitivity.

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Section: Discussionsupporting

confidence: 82%

Maternal High-Fat Diet Programs for Metabolic Disturbances in Offspring despite Leptin Sensitivity

et al. 2012

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“…Rodent models are important for understanding the relationship between HTG and the development of IR and glucose intolerance in the prediabetic state because prospective studies of diet on HTG concentrations can be easily designed and the effects are seen within a few days or weeks. Non-diabetic healthy rats placed on a HF diet accumulate HTG (9,10) and this is associated with significantly impaired insulin action, reduced whole-body glucose disposal rates, and hepatic IR (11)(12)(13)(14)(15). However, the time-scale and reversibility of HTG change induced by a HF diet and its associated effects on glucose homeostasis are less well defined in rats than in humans.…”

Section: Introductionmentioning

confidence: 96%

Sources of hepatic triglyceride accumulation during high‐fat feeding in the healthy rat

et al. 2008

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Hepatic triglyceride (HTG) accumulation from peripheral dietary sources and from endogenous de novo lipogenesis (DNL) was quantified in adult Sprague-Dawley rats by combining in vivo localized 1 H MRS measurement of total hepatic lipid with a novel ex vivo 2 H NMR analysis of HTG 2 H enrichment from 2 H-enriched body water. The methodology for DNL determination needs further validation against standard methodologies. To examine the effect of a high-fat diet on HTG concentrations and sources, animals (n ¼ 5) were given high-fat chow for 35 days. HTG accumulation, measured by in vivo 1 H MRS, increased significantly after 1 week (3.85 W 0.60% vs 2.13 W 0.34% for animals fed on a standard chow diet, P < 0.05) and was maintained until week 5 (3.30 W 0.60% vs 1.12 W 0.30%, P < 0.05). Animals fed on a high-fat diet were glucose intolerant (13.3 W 1.3 vs 9.4 W 0.8 mM in animals fed on a standard chow diet, for 60 min glycemia after glucose challenge, P < 0.05). In control animals, DNL accounted for 10.9 W 1.0% of HTG, whereas in animals given the high-fat diet, the DNL contribution was significantly reduced to 1.0 W 0.2% (P < 0.01 relative to controls). In a separate study to determine the response of HTG to weaning from a high-fat diet, animals with raised HTG (3.33 W 0.51%) after 7days of a high-fat diet reverted to basal HTG concentrations (0.76 W 0.06%) after an additional 7 days of weaning on a standard chow diet. These studies show that, in healthy rats, HTG concentrations are acutely influenced by dietary lipid concentrations. Although the DNL contribution to HTG content is suppressed by a high-fat diet in adult Sprague-Dawley rats, this effect is insufficient to prevent overall increases in HTG concentrations.

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“…The ob/ob mouse model develops steatosis spontaneously and has been well studied by 1 H-MRS (19)(20)(21)(22). Mice fed a high-fat or a high-fructose diet were also reported with steatosis ( 23,24 ).…”

Section: Mr Experimental Conditionsmentioning

confidence: 99%

In vivo hepatic lipid quantification using MRS at 7 Tesla in a mouse model of glycogen storage disease type 1a

Ramamonjisoa

Ratiney

Mutel

et al. 2013

Journal of Lipid Research

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This article is available online at http://www.jlr.org Glycogen storage disease type 1 (GSD 1) is an autosomal recessive metabolic disorder resulting in severe impairment of glucose production and large accumulation of lipids within hepatocytes (steatosis) ( 1, 2 ). The phenotype of GSD 1 results from a defect in the glucose-6 phosphatase (G6Pase) complex, leading to severe hypoglycemia due to the loss of endogenous glucose production. Despite a strict diet, patients with GSD 1 develop hepatomegaly and steatosis and may develop, with age, hepatocellular adenoma that can ultimately evolve into hepatocellular carcinoma ( 3, 4 ). Recently, a viable mouse model of GSD 1a with a liverspecifi c deletion of G6Pase catalytic subunit (L-G6pc Ϫ / Ϫ ) has been generated and validated ( 5 ). GSD 1a mice exhibit hepatic pathological features very similar to those observed in GSD 1a patients.The accumulation of lipids in the liver relates to the buildup of neutral lipids, such as triglycerides (TGs) and cholesterol esters, stored as lipid droplets in hepatocytes and leading to hepatic steatosis. This fat accumulation may originate from a ) peripheral fat stored in adipose tissue that fl ows to the liver as plasma nonesterifi ed fatty acids, b ) fatty acids newly made within the liver through de novo lipogenesis, and c ) dietary fatty acids ( 6, 7 ).Steatosis is highly linked to the development of metabolic diseases such as obesity or type 2 diabetes, but it can also result from genetic disorders impacting lipid and glucose metabolism such as in GSD 1a, ␣ 1-antitrypsin defi ciency, Abstract The assessment of liver lipid content and composition is needed in preclinical research to investigate steatosis and steatosis-related disorders. The purpose of this study was to quantify in vivo hepatic fatty acid content and composition using a method based on short echo time proton magnetic resonance spectroscopy (MRS) at 7 Tesla. A mouse model of glycogen storage disease type 1a with inducible liver-specifi c deletion of the glucose-6-phosphatase gene (L-G6pc ؊ / ؊ ) mice and control mice were fed a standard diet or a high-fat/high-sucrose (HF/HS) diet for 9 months. In control mice, hepatic lipid content was found signifi cantly higher with the HF/HS diet than with the standard diet. As expected, hepatic lipid content was already elevated in L-G6pc ؊ / ؊ mice fed a standard diet compared with control mice. L-G6pc ؊ / ؊ mice rapidly developed steatosis which was not modifi ed by the HF/HS diet. On the standard diet, estimated amplitudes from olefi nic protons were found signifi cantly higher in L-G6pc ؊ / ؊ mice compared with that in control mice. L-G6pc ؊ / ؊ mice showed no noticeable polyunsaturation from diallylic protons. Total unsaturated fatty acid indexes measured by gas chromatography were in agreement with MRS measurements. These results showed the great potential of high magnetic fi eld MRS to follow the diet impact and lipid alterations in mouse liver.

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Time course of the development of non-alcoholic hepatic steatosis in response to high-fat diet-induced obesity in rats

Cited by 104 publications

References 31 publications

Maternal High-Fat Diet Programs for Metabolic Disturbances in Offspring despite Leptin Sensitivity

Maternal High-Fat Diet Programs for Metabolic Disturbances in Offspring despite Leptin Sensitivity

Sources of hepatic triglyceride accumulation during high‐fat feeding in the healthy rat

In vivo hepatic lipid quantification using MRS at 7 Tesla in a mouse model of glycogen storage disease type 1a

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