Pathobiological and molecular connections involved in the high fructose and high fat diet induced diabetes associated nonalcoholic fatty liver disease

Ekta, .; Gupta, Manisha; Kaur, Amandeep; Singh, Thakur Gurjeet; Bedi, Onkar

doi:10.1007/s00011-020-01373-7

Cited by 13 publications

(6 citation statements)

References 155 publications

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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%

“…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%

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Effect of Probiotic Supplementation on Sprague Dawley Rat Liver Histopathology Fed by High Fat High Fructose Diet

Kusumawati

Panunggal

Mexitalia

et al. 2021

J. Biomed. Transl. Res.

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Background: Non-alcoholic fatty liver disease (NAFLD) is an important cause of liver disease burden worldwide. The gastrointestinal microbiota has a close relationship with the liver as the liver is most exposed to intestinal bacteria. Microbial manipulation is a potential and effective therapy as an alternative in the management of NAFLD/NASH. It has been found that probiotics prevent NAFLD/NASH. However, the study about the protective effect of probiotics on NAFLD/NASH is still limited. Objective: The objective of this study is to evaluate the effect of probiotics on liver histopathology Sprague Dawley rats which given high-fat high fructose (HFHFr) dietMethods: This study is a murine-model post-test-only control study group design. The samples were 21 Sprague Dawley male rats in 7 – 8 weeks of age and were divided into three groups. The Control Group (C) was provided with a standard chow diet for eight weeks. The Non-Probiotic (NP) group was given a High-Fat High Fructose (HFHFr) diet for eight weeks. The Probiotic group (P) was given a HFHFr diet for eight weeks, and a combination of HFHFr and probiotic supplementation consisted of Lactobacillus acidophilus, Bifidobacterium longum, and Streptococcus thermophilus for the next eight weeks. Histopathological samples were obtained from liver biopsy to assess steatosis, NAFLD activity score (NAS), and fibrosis stages. Wilcoxon test was done to analyze body weight before and after treatment. We analyzed the difference in histopathological results using the Mann-Whitney test.Results: We found a significant difference in NAFL and NAS Score between NP and P group. The P group was shown to have lower trends for NAFLD and NASH than the NP group, but not for fibrosis. There is no significant difference between pre and post-test body weight. Conclusion: Probiotics supplementation has a protective effect on liver histopathology against disturbances caused by the HFHFr diet.

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Section: Resultsmentioning

confidence: 63%

Section: Introductionmentioning

confidence: 99%

Effect of Probiotic Supplementation on Sprague Dawley Rat Liver Histopathology Fed by High Fat High Fructose Diet

Kusumawati

Panunggal

Mexitalia

et al. 2021

J. Biomed. Transl. Res.

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“…Prior to the diagnosis of pre-diabetes, there is a presence of insulin resistance and malfunctioning of pancreatic β-cells [185][186][187]. Studies show that diet high in saturated fats, high in carbohydrates or high in fructose contribute to the development of intermediate hyperglycemia [197][198][199]. In addition, studies also show that these high caloric food leads to elevated triglycerides, increase release of free fatty acid (FFA) from adipocytes into circulation, which is accompanied by decreased FFA uptake by adipocytes in insulin-dependent tissues promoting insulin resistance and dyslipidemia [200][201][202][203].…”

Section: Prediabetesmentioning

confidence: 99%

A Review of Fetal Development in Pregnancies with Maternal Type 2 Diabetes Mellitus (T2DM)‐ Associated Hypothalamic‐Pituitary‐Adrenal (HPA) Axis Dysregulation: Exploring Links to Pregestational Prediabetes

Ngema,

Xulu,

Ngubane

et al. 2024

Preprint

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A growing body of research has identified fetal risk factors associated with adult diseases that form the basis for the Developmental Origins of Health and Disease (DOHaD) hypothesis. This theory proposes a critical developmental period during which the fetus is highly susceptible to specific environmental influences that significantly impact health from short to long term. Maternal stress and T2DM during pregnancy are among these influences, likely leading to fetal overexposure to glucocorticoids and suggesting a shared pathway between maternal dysregulated HPA axis and fetal environmental insults. Studies demonstrate that prenatal glucocorticoid exposure alters fetal HPA axis function, affecting brain function, tissue glucocorticoid availability, and fetal growth in utero. These programmed changes, such as altered HPA axis function and reduced fetal growth, contribute to metabolic disorders persisting into adulthood. T2DM is preceded by a prediabetic state, often asymptomatic, which shares similar pathophysiological complications with T2DM, including HPA axis dysregulation observed in animals. Therefore, investigating prediabetes during pregnancy alongside maternal HPA axis function and its effects on fetal outcomes is crucial, as these areas remain understudied. This review aims to synthesize existing literature on pre-existing T2DM during pregnancy, its links to fetal programming via HPA axis changes, and possible links to pregestational prediabetes.

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“…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%

The “Adipo-Cerebral” Dialogue in Childhood Obesity: Focus on Growth and Puberty. Physiopathological and Nutritional Aspects

et al. 2021

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Overweight and obesity in children and adolescents are overwhelming problems in western countries. Adipocytes, far from being only fat deposits, are capable of endocrine functions, and the endocrine activity of adipose tissue, resumable in adipokines production, seems to be a key modulator of central nervous system function, suggesting the existence of an “adipo-cerebral axis.” This connection exerts a key role in children growth and puberty development, and it is exemplified by the leptin–kisspeptin interaction. The aim of this review was to describe recent advances in the knowledge of adipose tissue endocrine functions and their relations with nutrition and growth. The peculiarities of major adipokines are briefly summarized in the first paragraph; leptin and its interaction with kisspeptin are focused on in the second paragraph; the third paragraph deals with the regulation of the GH-IGF axis, with a special focus on the model represented by growth hormone deficiency (GHD); finally, old and new nutritional aspects are described in the last paragraph.

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Pathobiological and molecular connections involved in the high fructose and high fat diet induced diabetes associated nonalcoholic fatty liver disease

Cited by 13 publications

References 155 publications

Effect of Probiotic Supplementation on Sprague Dawley Rat Liver Histopathology Fed by High Fat High Fructose Diet

Effect of Probiotic Supplementation on Sprague Dawley Rat Liver Histopathology Fed by High Fat High Fructose Diet

A Review of Fetal Development in Pregnancies with Maternal Type 2 Diabetes Mellitus (T2DM)‐ Associated Hypothalamic‐Pituitary‐Adrenal (HPA) Axis Dysregulation: Exploring Links to Pregestational Prediabetes

The “Adipo-Cerebral” Dialogue in Childhood Obesity: Focus on Growth and Puberty. Physiopathological and Nutritional Aspects

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