Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress

Veličković, Nataša; Teofilović, Ana; Ilić, D.; Djordjević, Ana; Milutinović, Danijela Vojnović; Petrović, Snježana; Preitner, Frédéric; Tappy, Luc; Matić, Gordana

doi:10.1007/s00394-018-1730-1

Cited by 14 publications

(12 citation statements)

References 73 publications

(87 reference statements)

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“…Our results are in agreement with those of previous studies showing that high fructose intake reduces nutrient-sensing signals [ 28 , 29 ]. Probiotic therapy has nearly no effect on renal nutrient-sensing signals at both mRNA and protein levels.…”

Section: Discussionsupporting

confidence: 94%

Maternal Administration of Probiotic or Prebiotic Prevents Male Adult Rat Offspring against Developmental Programming of Hypertension Induced by High Fructose Consumption in Pregnancy and Lactation

et al. 2018

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Excessive intake of fructose is associated with hypertension. Gut microbiota and their metabolites are thought to be associated with the development of hypertension. We examined whether maternal high-fructose (HF) diet-induced programmed hypertension via altering gut microbiota, regulating short-chain fatty acids (SCFAs) and their receptors, and mediating nutrient-sensing signals in adult male offspring. Next, we aimed to determine whether early gut microbiota-targeted therapies with probiotic Lactobacillus casei and prebiotic inulin can prevent maternal HF-induced programmed hypertension. Pregnant rats received 60% high-fructose (HF) diet, with 2 × 108 CFU/day Lactobacillus casei via oral gavage (HF+Probiotic), or with 5% w/w long chain inulin (HF+prebiotic) during pregnancy and lactation. Male offspring (n = 7–8/group) were assigned to four groups: control, HF, HF+Probiotic, and HF+Prebiotic. Rats were sacrificed at 12 weeks of age. Maternal probiotic Lactobacillus casei and prebiotic inulin therapies protect against hypertension in male adult offspring born to fructose-fed mothers. Probiotic treatment prevents HF-induced hypertension is associated with reduced plasma acetate level and decreased renal mRNA expression of Olfr78. While prebiotic treatment increased plasma propionate level and restored HF-induced reduction of Frar2 expression. Maternal HF diet has long-term programming effects on the adult offspring’s gut microbiota. Probiotic and prebiotic therapies exerted similar protective effects on blood pressure but they showed different mechanisms on modulation of gut microbiota. Maternal HF diet induced developmental programming of hypertension, which probiotic Lactobacillus casei or prebiotic inulin therapy prevented. Maternal gut microbiota-targeted therapies could be reprogramming strategies to prevent the development of hypertension caused by maternal consumption of fructose-rich diet.

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Section: Discussionsupporting

confidence: 94%

Maternal Administration of Probiotic or Prebiotic Prevents Male Adult Rat Offspring against Developmental Programming of Hypertension Induced by High Fructose Consumption in Pregnancy and Lactation

et al. 2018

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“…In our experiments, CS alone increased blood glucose concentrations, but had no significant effect on glucose tolerance [28] or on intrahepatic/intrarenal fat, fDNL, or VLDL-TG secretion. In contrast, the combined CS and HFr enhanced hypertriglyceridemia and fDNL-VLDL, while CS additionally potentiated the effects of HFr on increased IRTG-DNPalm content at the end of the feeding phase.…”

Section: Discussioncontrasting

confidence: 59%

“…Nevertheless, impaired glucose tolerance, which is a hallmark of hepatic and systemic insulin resistance, and increased inhibitory phosphorylation of IRS1 in hepatocyte, which is a marker of hepatic insulin resistance, were previously observed in HFr animals. [28] Noteworthy, in this former study, hyperinsulinemia and hypoglycemia were observed in HFr animals, which is most likely a result of overnight fasting. [29] In the current study, HFr increased the expression of fructose transporters and fructolysis enzymes in both liver and kidney, as well as renal expression of gluconeogenic genes, indicating that whatever portion of fructose escaped firstpass splanchnic uptake, it was sufficient to up-regulate fructose and glucose metabolism in the kidney.…”

Section: Discussionmentioning

confidence: 57%

“…CS thus boosted the effects of HFr on VLDL-DNPalm secretion and plasma VLDL-TG, but at the same time temporarily decreasing IHTG storage during the feeding phase, which suggests that newly made palmitate was channeled into the circulation rather than being sequestered in the liver. This may be explained by increased glucocorticoids evoked by chronic stress, [24] since these hormones promote both hepatic TG synthesis and their release as VLDL. [46] In our study, stress significantly increased mRNA level of MTTP, which is a key player in the assembly and secretion of hepatic VLDL.…”

Section: Discussionmentioning

confidence: 99%

“…Preparation of cell extracts for Western blot analysis was done as previously published. [24] The used primary antibodies are listed in Table S1 (Supporting Information). Membranes were subsequently washed and incubated with anti-rabbit (NA934, 1:20000, GE Healthcare) or anti-mouse (ab97046, 1:30000, Abcam) HRPconjugated secondary antibodies.…”

Section: Western Blot Analysismentioning

confidence: 99%

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Chronic Stress Potentiates High Fructose–Induced Lipogenesis in Rat Liver and Kidney

Milutinović

Brkljačić

Teofilović

et al. 2020

Molecular Nutrition Food Res

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Scope Intake of fructose‐sweetened beverages and chronic stress (CS) both increase risk of cardiometabolic diseases. The aim is to investigate whether these factors synergistically perturb lipid metabolism in rat liver and kidney. Methods and results Fractional de novo lipogenesis (fDNL), intrahepatic‐ and intrarenal‐triglycerides (IHTG and IRTG), de novo palmitate (DNPalm) content, FA composition, VLDL‐TGs kinetics, and key metabolic gene expression at the end of the feeding and non‐feeding phases in rats exposed to standard chow diet, chow diet + CS, 20% liquid high‐fructose supplementation (HFr), or HFr+CS are measured. HFr induces hypertriglyceridemia, up‐regulates fructose‐metabolism and gluconeogenic enzymes, increases IHTG and DNPalm content in IHTG and IRTG, and augments fDNL at the end of the feeding phase. These changes are diminished after the non‐feeding phase. CS does not exert such effects, but when combined with HFr, it reduces IHTG and visceral adiposity, enhances lipogenic gene expression and fDNL, and increases VLDL‐DNPalm secretion. Conclusion Liquid high‐fructose supplementation increases IHTG and VLDL‐TG secretion after the feeding phase, the latter being the result of stimulated hepatic and renal DNL. Chronic stress potentiates the effects of high fructose on fDNL and export of newly synthesized VLDL‐TGs, and decreases fructose‐induced intrahepatic TG accumulation after the feeding phase.

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Glucocorticoid signaling and lipid metabolism disturbances in the liver of rats treated with 5α-dihydrotestosterone in an animal model of polycystic ovary syndrome

et al. 2021

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Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress

Cited by 14 publications

References 73 publications

Maternal Administration of Probiotic or Prebiotic Prevents Male Adult Rat Offspring against Developmental Programming of Hypertension Induced by High Fructose Consumption in Pregnancy and Lactation

Maternal Administration of Probiotic or Prebiotic Prevents Male Adult Rat Offspring against Developmental Programming of Hypertension Induced by High Fructose Consumption in Pregnancy and Lactation

Chronic Stress Potentiates High Fructose–Induced Lipogenesis in Rat Liver and Kidney

Glucocorticoid signaling and lipid metabolism disturbances in the liver of rats treated with 5α-dihydrotestosterone in an animal model of polycystic ovary syndrome

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