Activity of glycogen synthase and glycogen phosphorylase in normal and cirrhotic rat liver during glycogen synthesis from glucose or fructose

Bezborodkina, Natalia N.; Chestnova, Anna Yu.; Okovity, Sergey V.; Kudryavtsev, B. N.

doi:10.1016/j.etp.2013.12.001

Cited by 21 publications

(7 citation statements)

References 39 publications

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“…Glycogen accumulation in human cirrhotic hepatocytes was accompanied by a marked decrease in GP and GPa activity, by 22% and by 46%, respectively ( Figure 6 B). This result confirms our earlier data [ 14 , 18 , 35 ]. We conclude that the abatement of glycogenolysis due to a low activity of GPa may be an important mechanism of increasing glycogen concentration in the cirrhotic human liver.…”

Section: Discussionsupporting

confidence: 94%

“…GS activity was estimated by the amount of [U- 14 C]glucose included in the glycogen, using UDP-[U- 14 C]glucose (300 mCi/mM) as a substrate; GP activity was determined using the inverse reaction of glycogen synthesis in vitro using [U- 14 C]glucose-1-phosphate (286 mCi/mM) as a substrate [ 17 , 18 ]. The number of impulses was registered with a counter (Beckman, Indianapolis, IN, USA).…”

Section: Methodsmentioning

confidence: 99%

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Postprandial Glycogen Content Is Increased in the Hepatocytes of Human and Rat Cirrhotic Liver

Bezborodkina

Оковитый

Kudryavtsev

2021

Cells

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Chronic hepatitises of various etiologies are widespread liver diseases in humans. Their final stage, liver cirrhosis (LC), is considered to be one of the main causes of hepatocellular carcinoma (HCC). About 80–90% of all HCC cases develop in LC patients, which suggests that cirrhotic conditions play a crucial role in the process of hepatocarcinogenesis. Carbohydrate metabolism in LC undergoes profound disturbances characterized by altered glycogen metabolism. Unfortunately, data on the glycogen content in LC are few and contradictory. In this study, the material was obtained from liver biopsies of patients with LC of viral and alcohol etiology and from the liver tissue of rats with CCl4-induced LC. The activity of glycogen phosphorylase (GP), glycogen synthase (GS), and glucose-6-phosphatase (G6Pase) was investigated in human and rat liver tissue by biochemical methods. Total glycogen and its labile and stable fractions were measured in isolated individual hepatocytes, using the cytofluorometry technique of PAS reaction in situ. The development of LC in human and rat liver was accompanied by an increase in fibrous tissue (20- and 8.8-fold), an increase in the dry mass of hepatocytes (by 25.6% and 23.7%), and a decrease in the number of hepatocytes (by 50% and 28%), respectively. The rearrangement of the liver parenchyma was combined with changes in glycogen metabolism. The present study showed a significant increase in the glycogen content in the hepatocytes of the human and the rat cirrhotic liver, by 255% and 210%, respectively. An increased glycogen content in cells of the cirrhotic liver can be explained by a decrease in glycogenolysis due to a decreased activity of G6Pase and GP.

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Section: Discussionsupporting

confidence: 94%

Section: Methodsmentioning

confidence: 99%

Postprandial Glycogen Content Is Increased in the Hepatocytes of Human and Rat Cirrhotic Liver

Bezborodkina

Оковитый

Kudryavtsev

2021

Cells

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“…In humans, fructose intake rapidly increases post-exercise liver glycogen synthesis ( Décombaz et al, 2011 ). In rats, administration of fructose causes an immediate increase of glycogen synthase (GS) activity and initiates a fast accumulation of glycogen in the liver ( Bezborodkina et al, 2014 ). Actually, glucose is usually used in food processing in a ratio of nearly 1:1 with fructose, high levels of glucose in the portal vein can induce the expression of hepatic aldose reductase (AR), resulting in the conversion of glucose into sorbitol, which is then metabolized to fructose by sorbitol dehydrogenase ( Lanaspa et al, 2013 ).…”

Section: Fructose Metabolism In the Development Of Nashmentioning

confidence: 99%

The Contribution of Dietary Fructose to Non-alcoholic Fatty Liver Disease

Yu¹,

Li²,

Ji³

et al. 2021

Front. Pharmacol.

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Fructose, especially industrial fructose (sucrose and high fructose corn syrup) is commonly used in all kinds of beverages and processed foods. Liver is the primary organ for fructose metabolism, recent studies suggest that excessive fructose intake is a driving force in non-alcoholic fatty liver disease (NAFLD). Dietary fructose metabolism begins at the intestine, along with its metabolites, may influence gut barrier and microbiota community, and contribute to increased nutrient absorption and lipogenic substrates overflow to the liver. Overwhelming fructose and the gut microbiota-derived fructose metabolites (e.g., acetate, butyric acid, butyrate and propionate) trigger the de novo lipogenesis in the liver, and result in lipid accumulation and hepatic steatosis. Fructose also reprograms the metabolic phenotype of liver cells (hepatocytes, macrophages, NK cells, etc.), and induces the occurrence of inflammation in the liver. Besides, there is endogenous fructose production that expands the fructose pool. Considering the close association of fructose metabolism and NAFLD, the drug development that focuses on blocking the absorption and metabolism of fructose might be promising strategies for NAFLD. Here we provide a systematic discussion of the underlying mechanisms of dietary fructose in contributing to the development and progression of NAFLD, and suggest the possible targets to prevent the pathogenetic process.

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“…Adipose and hepatic glycogen concentration and glycogen synthase activity were determined as previously described (Vilkova 1982, Vardanis 1992, Bezborodkina et al 2014) using standard non-enzymatic and enzymatic spectrophotometric methods, respectively, and reagents obtained from Oxford Biomedical Research.…”

Section: Glycogen Concentration and Glycogen Synthase Activitymentioning

confidence: 99%

L-glutamine ameliorates adipose-hepatic dysmetabolism in OC-treated female rats

Olaniyi

Olatunji

2020

Journal of Endocrinology

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Adipose dysfunction and inflammation with or without hepatic defects underlie metabolic obesity. Glutamine (GLU) improves glucoregulation and metabolic indices but its effects on adipose function and hepatic lipid deposition in estrogen-progestin oral contraceptive (EPOC) users are unknown. Therefore, we hypothesized that GLUT supplementation would protect against adipose dysfunction and excess hepatic lipid influx and deposition in EPOC-treated animals by suppressing adenosine deaminase/xanthine oxidase (ADA/XO) activity and improving glucose-6-phosphate dehydrogenase (G6PD)-dependent antioxidant defense. Female Wistar rats weighing 150–180 g were allotted into control, GLUT, EPOC and EPOC + GLUT groups (six rats/group). The groups received vehicle (distilled water, p.o.), GLUT (1 g/kg), EPOC containing 1.0 µg ethinylestradiol plus 5.0 µg levonorgestrel and EPOC plus GLUT, respectively, daily for 8 weeks. Results showed that the administration of EPOC caused glucose dysregulation and increased triglyceride-glucose index and visceral adiposity, but the body weight and liver weight were not affected. However, EPOC significantly decreased adipose lipid, G6PD and glutathione and increased glycogen synthesis, ADA, XO, uric acid, lipid peroxidation, lactate production and gamma-glutamyl transferase activity (GGT). On the other hand, EPOC increased hepatic lipid, ADA, XO, uric acid, lipid peroxidation and lactate production and decreased glycogen synthesis, G6PD and glutathione. Nevertheless, supplementation with glutamine attenuated these alterations. Collectively, the present results indicate that EPOC causes metabolically induced obesity which is associated with adipose dysfunction and hepatic metabolic disturbance. The findings also suggest that glutamine confers metabo-protection with corresponding improvement in adipose and hepatic metabolic function by suppression of ADA/XO activity and enhancement of G6PD-dependent antioxidant defense.

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Activity of glycogen synthase and glycogen phosphorylase in normal and cirrhotic rat liver during glycogen synthesis from glucose or fructose

Cited by 21 publications

References 39 publications

Postprandial Glycogen Content Is Increased in the Hepatocytes of Human and Rat Cirrhotic Liver

Postprandial Glycogen Content Is Increased in the Hepatocytes of Human and Rat Cirrhotic Liver

The Contribution of Dietary Fructose to Non-alcoholic Fatty Liver Disease

L-glutamine ameliorates adipose-hepatic dysmetabolism in OC-treated female rats

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