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A low-carbohydrate diet induces hepatic insulin resistance and metabolic-associated fatty liver disease

ABSTRACT: A low-carbohydrate diet induces hepatic insulin resistance and metabolic-associated fatty liver disease

PROVIDER: PRJNA901940 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22301117.fastq.gz	Fastqsanger.gz
	SRR22301118.fastq.gz	Fastqsanger.gz
	SRR22301119.fastq.gz	Fastqsanger.gz
	SRR22301120.fastq.gz	Fastqsanger.gz
	SRR22301121.fastq.gz	Fastqsanger.gz

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A low-carbohydrate diet induces hepatic insulin resistance and metabolic-associated fatty liver disease

Project description:We demonstrate that the ketogenic diet a low carbohydrate diet can induce fibrosis and NASH regardless of body weight loss compared to high-fat diet (HFD) fed mice. KD-fed mice develop severe hepatic injury, inflammation, and steatosis. In addition, KD increases IL-6-JNK signaling and aggravates diet induced-glucose intolerance and hepatic insulin resistance compared to HFD. Notably, pharmacological inhibition of IL-6 and JNK reverses KD‐induced glucose intolerance and restores insulin sensitivity.

2023-01-31 | GSE218025 | GEO

Hepatic insulin resistance promotes fructose-enriched diet-induced fatty liver diseases.

Project description:Understanding mechanisms causing MAFLD (Metabolic Associated Fatty Liver Disease) and its progression to MASH (metabolic dysfunction-associated steatohepatitis) is clinically important and scientifically challenging. Hepatic insulin resistance is a common component in the progression of MAFLD in patients and experimental animals; however, hepatic steatosis caused by the HFD45% (high-fat diet) decreases during chronic hepatic IR generated by inactivation of Irs1/2 (LDKO), AKT1/2, or InsR 1-3—which is inconsistent with the expected relationship between IR and MAFLD in humans4. Here we found that complete hepatic insulin resistance promotes the fructose-enriched GAN diet-induced MAFLD, including acute inflammation and MASH in LDKO mice. Unexpectedly, fructose phosphorylation catalyzed by hepatic Khk (ketohexokinase) was not required as acute MAFLD progressed strongly in LDKOKhkL/L mice fed the GAN diet. FoxO1 activated during hepatic IR induces Fst (Follistatin) expression and secretion from the liver of LDKO mice. Inactivation of hepatic FoxO1 in LTKO mice (LDKO•FoxO1L/L) or Fst in LDKOFstKO mice prevented acute MAFLD during the GAN diet. Consistently, overexpression of hepatic Fst promoted GAN diet-induced MAFLD/MASH and hepatic carcinoma. Mechanistically, circulating Fst promoted adipose tissue IR and lipolysis, which can deliver FFA (free fatty acid) to the liver for esterification with excess Gro3P (glycerol 3-phosphate) generated by fructose metabolism, although hepatic DNL (de novo lipogenesis) decreased strongly in LDKO mice while. Since circulating FST correlates positively with both T2D and MAFLD in humans, our results suggests that hepatic FST induced by progressive hepatic IR might promote MAFLD/MASH during the consumption of sugar-sweetened food and beverages consumed frequently by people and animals with T2D.

2024-06-23 | GSE270246 | GEO

Hepatic insulin resistance promotes fructose-enriched diet-induced fatty liver diseases.

Project description:Hepatic insulin resistance promotes fructose-enriched diet-induced fatty liver diseases.

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The Effect of Fatty Acids in Hepatic Insulin Resistance - Part 1

Project description:Monounsaturated fatty acid (MUFA) oleic acid (OA) has been reported to restore saturated fatty acid palmitic acid (PA)-induced hepatic insulin resistance (IR). However, the detailed molecular mechanism remains elusive. In addition, -3 polyunsaturated fatty acid (PUFA) such as Eicosapentaenoic acid (EPA) has also exerted opposite effects to PA in muscle IR. But whether it plays the same role in hepatic IR and the possible mechanism involved needs to be further explored. Here, we compared the proteome change of HepG2 cells after different fatty acids treatment.

2019-07-11 | PXD012065 | Pride

Low carbohydrate diet study for non-alcoholic fatty liver disease patients

Project description:Low carbohydrate diet study for non-alcoholic fatty liver disease patients

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Low carbohydrate diet study for non-alcoholic fatty liver disease patients

Project description:We performed a short-term dietary intervention with a low-carbohydrate diet in obese subjects with NAFLD

2018-02-15 | GSE107650 | GEO

A Maternal low protein diet differentially programs glucose and fatty acid metabolism in adult male and female offspring

Project description:Analysis of glucose and Lipid metabolism in male and female offspring after protein restriction of the mother Male offspring showed features of metabolic syndrome after receiving a high fat diet, regardless of the diet of the dam. Glucose and lipid metabolism in male offspring was unaltered. Insulin sensitivity and hepatic fatty acid storage in female offspring of low-protein-fed dams changed in such a way that it resembled the male pattern of insulin sensitivity and hepatic fatty acid storage. Microarray analysis on hepatic gene expression patterns confirmed these findings. We therefore conclude that in mice, maternal protein restriction does not change the response of glucose and fatty acid metabolism to a high fat diet in male offspring, but does program metabolism in female offspring in such a way that it resembles male metabolism. Our findings might have implications for potential future gender-specific treatment of the features of metabolic diseases. Total RNA obtained from liver (16 samples per gender) were compared in the different groups. In total, 4 groups per gender, each group consisting of 4 biological replicates.

2012-02-08 | E-GEOD-15940 | biostudies-arrayexpress

Low dose perfluorooctanesulfonic acid (PFOS) and perfluorohexanesulfonic acid (PFHxS) augment hepatic steatosis and shift the sera lipidome in a high fat high carbohydrate diet.

Project description:Non-alcoholic fatty liver disease (NAFLD) is most prevalent form of liver disease, affecting over 30% of Americans. Perfluoroalkyl substances (PFAS) represent a family of environmental toxicants that have infiltrated the living world. This study explores diet-PFAS interactions and their potential role in the increasing global incidence of NAFLD. Male C57BL/6 mice were fed with either a low-fat diet (11% kcal from fat) or a high fat (58% kcal from fat) high carbohydrate (42g/L) diet with or without PFOS or PFHxS in feed (0.0003% w/w) for 29 weeks. Proteomic, lipidomic, and gene expression measurement techniques were utilized to explore mechanistic pathways. With administration of a high fat high carbohydrate (HFHC) diet, PFOS and PFHxS augmented macrovesicular steatosis, indicative of fatty liver. There was a clear shift in the lipidome of the serum phosphatidylcholines, phosphatidylethanolamines, and triglycerides with PFAS exposure. Finally, chain length exerted significant influence on tissue partitioning and the resulting hepatic gene and protein signatures of PFHxS and PFOS in vivo.

2020-09-15 | PXD015976 | Pride

the Effect of Fatty Acids in Hepatic Insulin resistance-part2

Project description:Monounsaturated fatty acid (MUFA) oleic acid (OA) has been reported to reverse saturated fatty acid palmitic acid (PA)-induced hepatic insulin resistance (IR). However, the detailed molecular mechanism remains elusive. In addition, previous research also showed that -3 polyunsaturated fatty acid (PUFA) eicosapentaenoic acid (EPA), exerted opposite effects to PA in muscle IR, but whether it plays the same role in hepatic IR and the possible mechanism involved needs to be further explored. Here, we confirmed that EPA reversed PA-induced IR in HepG2 cells and compared the proteome change after different free fatty acids (FFAs) treatments. For MUFA, 234 proteins were identified as differentially expressed proteins, and their functions were mainly related to response to stress and endogenous stimuli, lipid metabolic process and protein binding. For PUFA, the PA-induced expression change of 1326 proteins could be reversed by EPA and 415 of them were mitochondrial proteins, which covered most of the functional proteins in oxidative phosphorylation (OXPHOS) and tricarboxylic acid cycle (TCA). Mechanism study revealed that c-Jun and ROS played a role in OA- and EPA-reversed PA-induced IR, respectively. EPA or OA alleviated PA-induced abnormal ATP production, ROS generation, and calcium content. Importantly, H2O2-activated production of ROS increased the expression of c-Jun, further resulting in IR of HepG2 cells. Besides, we provided more feasible candidates as potential c-Jun-targeted “responders” for FFAs treatments. Taken together, we demonstrated that ROS/c-Jun is a common pathway to different FFAs-regulated IR in HepG2 cells.

2019-07-11 | PXD012066 | Pride

Programming of the hepatic lipid metabolism via a parental high carbohydrate low protein diet in rainbow trout

Project description:In rainbow trout (Oncorhynchus mykiss), the effect of a paternal and a maternal high carbohydrate-low protein diet was assessed on progeny at long term. To this purpose, two-year old male and female rainbow trout were fed either a control diet or a high carbohydrate/low protein diet for an entire reproductive cycle for females and for 5 months for males. Crossed-fertilizations were carried out in order to obtain 4 groups of offspring. Offspring were fed with a commercial diet until they reached a market size and were then challenged with a complete plant-based diet for 3 months. After the challenge, hepatic transcriptomes were analysed to detect any effect of the parental diet on offspring metabolism.

2022-07-31 | GSE184632 | GEO

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