2020
DOI: 10.1007/s00011-020-01373-7
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Pathobiological and molecular connections involved in the high fructose and high fat diet induced diabetes associated nonalcoholic fatty liver disease

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Cited by 8 publications
(4 citation statements)
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“…Our control group did not develop NAFLD and NASH, although rats in those groups developed stage I fibrosis. We also found that in the probiotic group, there were fewer subjects developing NAFLD (see table 3), NASH (see table 4), and stage II fibrosis (see table 5) Fisher's Exact analysis showed that compared to the NP group, the P group was shown to have lower trends for NAFLD (p = 0.001) and NASH (p = 0.001). It is shown that the P group had a lower trend for the fibrosis stage, although not statistically significant.…”
Section: Resultsmentioning
confidence: 63%
See 1 more Smart Citation
“…Our control group did not develop NAFLD and NASH, although rats in those groups developed stage I fibrosis. We also found that in the probiotic group, there were fewer subjects developing NAFLD (see table 3), NASH (see table 4), and stage II fibrosis (see table 5) Fisher's Exact analysis showed that compared to the NP group, the P group was shown to have lower trends for NAFLD (p = 0.001) and NASH (p = 0.001). It is shown that the P group had a lower trend for the fibrosis stage, although not statistically significant.…”
Section: Resultsmentioning
confidence: 63%
“…This type of diet also gives rise for endoplasmic reticulum stress, promoting mitochondrial dysfunction and elevating hepatocytes apoptosis. 4,5 Alterations in gut microbiota composition and function negatively impacts the host (dysbiosis) and play causal roles in developing NAFLD. 6 As the liver receives major blood supply from the intestine, it has a particular susceptibility of intestinal microbiota metabolite.…”
Section: Introductionmentioning
confidence: 99%
“…The rich consumption of fructose, commonly underestimated, leads to pro-inflammatory signaling by the release in various adipokines, correlated to IR and consequently to an overexpansion of adipose tissue [174]. Chen et al reported that excessive energy intake from fructose may elicit mitochondrial OS and decrease Thioredoxin 2 abundance, which is a vital factor for the viability of cells [175], and alters GLUT5, a major co-transporter of glucose, thereby promoting IR [176]. Sugar-sweetened drinks, such as carbonated soda, energy drinks, and highly sweetened coffees and teas, are frequently taken by adolescents, favoring fat deposition.…”
Section: Dietary Approach: the Role Of Carbohydrate And Fat Intakementioning
confidence: 99%
“…Fat intake has to be considered too. Indeed, high fat intake is directly correlated with hepatic IR due to the activation of protein kinases that impair glucose uptakes in adipocytes and muscles [176].…”
Section: Dietary Approach: the Role Of Carbohydrate And Fat Intakementioning
confidence: 99%