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A water-soluble polysaccharide (EP) was purified from edible algae Enteromorpha prolifera. Gel permeation chromatography (GPC), ion chromatography (IC), and fourier transform infrared (FT-IR) were performed to characterize its structure. EP was defined as a low molecular weight (6625 Da) composed of rhamnose, glucose, glucuronic acid, xylose, galactose, arabinose, and mannose. Moreover, it was a sulfated polysaccharide with a degree of substitution (DS) of 1.48. Then, the high-fat diet/streptozotocin (HFD/STZ) induced diabetic mouse model was established to support evidence for a novel hypoglycemic mechanism. Results showed that blood glucose (47.32%), liver index (7.65%), epididymal fat index (16.86%), serum total cholesterol (26.78%) and triglyceride (37.61%) in the high-dose EP (HEP) group were significantly lower than those in the HFD group. Noticeably, the content of liver glycogen in the HEP group was significantly higher (62.62%) than that in the HFD group, indicating the promotion of glycogen synthesis. These beneficial effects were attributed to significantly increased protein kinase B (AKT) phosphorylation and its downstream signaling response. Further studies showed that diabetic mice exhibited excessive O-GlcNAcylation level and high expression of O-linked β-D-N-acetylglucosamine transferase (OGT), which were decreased by 62.21 and 30.43% in the HEP group. This result suggested that EP had a similar effect to OGT inhibitors, which restored AKT phosphorylation and prevented pathoglycemia. This work reveals a novel hypoglycemic mechanism of EP, providing a theoretical basis for further studies on its pharmacological properties in improvement of T2DM. [ABSTRACT FROM AUTHOR]

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A trend in large yellow croaker (Larimichthys crocea) aquaculture is to establish production sites suitable for extreme weather conditions. However, continuous and strong currents can harm fish welfare. To determine a suitable site location, the swimming ability of large yellow croakers must be assessed. This study aims to provide novel insights into the physiological characteristics of large yellow croaker swimming and a reference for fishing and cage site selection. Currently, research on large yellow croakers has focused on behavior analysis. Herein, we investigate the effects of swimming on large yellow croakers' metabolites by examining the preferred speed of the group and the sustained swimming ability of single-tailed fish. We evaluated factors that influence the large yellow croaker's swimming fatigue by quantifying the metabolite contents and constructing a sustained swimming model. The results showed that large yellow croaker populations tend to grow in low-velocity environments, similar to their traditional habitat. The samples were taken at different swimming times at a flow velocity of 0.35 m/s. According to the results of the metabolite content analysis, blood glucose levels are closely associated with the swimming ability in large yellow croakers. The content of liver glycogen, which regulates blood glucose concentration, decreased in a certain linear relationship. The sustained swimming model of the large yellow croaker was constructed according to the changes in liver glycogen content. Based on our findings, we recommend the following: (1) for large yellow croakers with a size of approximately 13.5 cm (approximately 1 year old), the water velocity inside the cage should not exceed 2.6 BL/s; (2) the concentration of liver glycogen limits the sustained swimming ability of the large yellow croaker, providing a reference for studying the swimming ability of other fish. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: Time-restricted eating (TRE) is suggested to improve metabolic health by limiting food intake to a defined time window, thereby prolonging the overnight fast. This prolonged fast is expected to lead to a more pronounced depletion of hepatic glycogen stores overnight and might improve insulin sensitivity due to an increased need to replenish nutrient storage. Previous studies showed beneficial metabolic effects of 6–8 h TRE regimens in healthy, overweight adults under controlled conditions. However, the effects of TRE on glucose homeostasis in individuals with type 2 diabetes are unclear. Here, we extensively investigated the effects of TRE on hepatic glycogen levels and insulin sensitivity in individuals with type 2 diabetes. Methods: Fourteen adults with type 2 diabetes (BMI 30.5±4.2 kg/m2, HbA1c 46.1±7.2 mmol/mol [6.4±0.7%]) participated in a 3 week TRE (daily food intake within 10 h) vs control (spreading food intake over ≥14 h) regimen in a randomised, crossover trial design. The study was performed at Maastricht University, the Netherlands. Eligibility criteria included diagnosis of type 2 diabetes, intermediate chronotype and absence of medical conditions that could interfere with the study execution and/or outcome. Randomisation was performed by a study-independent investigator, ensuring that an equal amount of participants started with TRE and CON. Due to the nature of the study, neither volunteers nor investigators were blinded to the study interventions. The quality of the data was checked without knowledge on intervention allocation. Hepatic glycogen levels were assessed with 13C-MRS and insulin sensitivity was assessed using a hyperinsulinaemic–euglycaemic two-step clamp. Furthermore, glucose homeostasis was assessed with 24 h continuous glucose monitoring devices. Secondary outcomes included 24 h energy expenditure and substrate oxidation, hepatic lipid content and skeletal muscle mitochondrial capacity. Results: Results are depicted as mean ± SEM. Hepatic glycogen content was similar between TRE and control condition (0.15±0.01 vs 0.15±0.01 AU, p=0.88). M value was not significantly affected by TRE (19.6±1.8 vs 17.7±1.8 μmol kg−1 min−1 in TRE vs control, respectively, p=0.10). Hepatic and peripheral insulin sensitivity also remained unaffected by TRE (p=0.67 and p=0.25, respectively). Yet, insulin-induced non-oxidative glucose disposal was increased with TRE (non-oxidative glucose disposal 4.3±1.1 vs 1.5±1.7 μmol kg−1 min−1, p=0.04). TRE increased the time spent in the normoglycaemic range (15.1±0.8 vs 12.2±1.1 h per day, p=0.01), and decreased fasting glucose (7.6±0.4 vs 8.6±0.4 mmol/l, p=0.03) and 24 h glucose levels (6.8±0.2 vs 7.6±0.3 mmol/l, p<0.01). Energy expenditure over 24 h was unaffected; nevertheless, TRE decreased 24 h glucose oxidation (260.2±7.6 vs 277.8±10.7 g/day, p=0.04). No adverse events were reported that were related to the interventions. Conclusions/interpretation: We show that a 10 h TRE regimen is a feasible, safe and effective means to improve 24 h glucose homeostasis in free-living adults with type 2 diabetes. However, these changes were not accompanied by changes in insulin sensitivity or hepatic glycogen. Trial registration: ClinicalTrials.gov NCT03992248 Funding: ZonMW, 459001013 [ABSTRACT FROM AUTHOR]

Water temperature is the major ecophysiological factor for fish survival in nature and aquaculture. Compared with many homeotherms, fish can survive prolonged periods under the condition of low temperature. However, the metabolic strategies of the liver under a cold environment are still unknown in this species. In our present study, adult zebrafish were exposed to a cold or cold plus starvation environment to analyse the morphological characteristics of hepatocytes by light microscopy and transmission electron microscopy (TEM). The fish livers were dissected and observed under a microscope, and the liver size and shape appeared normal in all groups. Periodic acid‐Schiff and TEM analysis showed that hepatic glycogen was significantly lower in zebrafish exposed to cold acclimation (CF group) than that zebrafish at the control water temperature (CT group). Moreover, qPCR and IHC results indicated that the expression of PYGL (a key enzyme involved in glycogenolysis) markedly increased in the CF group. After cold plus starvation treatment (CS group), autophagy activity was significantly enhanced and numerous mitophagic vacuoles were present in the cytoplasm of hepatocytes. In conclusion, hepatic glycogen was first mobilizing to supply energy, and then autophagy, especially mitophagy, played vital roles during nutrient deprivation in fish species. [ABSTRACT FROM AUTHOR]

The hypothalamus is a major integrating centre that controls energy homeostasis and plays a major role in hepatic glycogen (HGlyc) turnover. Not only do hypothalamic and hepatic Akt levels influence glucose homeostasis and glycogen synthesis, but exposure to high-sugar/high-fat diets (HSHF) can also lead to hypothalamic inflammation and HGlyc accumulation. HSHF withdrawal overall restores energy and glucose homeostasis, but the actual relationship between hypothalamic inflammation and HGlyc after short-term HSHF withdrawal has not yet been fully elucidated. Here we investigated the short-term effects of HSHF withdrawal preceded by a 30-day HSHF intake on the liver-hypothalamus crosstalk and glucose homeostasis. Sixty-day old male Wistar rats were fed for 30 days a control chow (n = 10) (Ct), or an HSHF diet (n = 20). On the 30th day of dietary intervention, a random HSHF subset (n = 10) had their diets switched to control chow for 48 h (Hw) whilst the remaining HSHF rats remained in the HSHF diet (n = 10) (Hd). All rats were anaesthetized and euthanized at the end of the protocol. We quantified HGlyc, Akt phosphorylation, inflammation and glucose homeostasis biomarkers. We also assessed the effect of propensity to obesity on those biomarkers, as detailed previously. Hd rats showed impaired glucose homeostasis, higher HGlyc and hypothalamic inflammation, and lower pAkt/Akt. Increased HGlyc was significantly associated with HSHF intake on pAkt/Akt lowered levels. We also found that HGlyc breakdown may have prevented a further pAkt/Akt drop after HSHF withdrawal. Propensity to obesity showed no apparent effect on hypothalamic inflammation or glucose homeostasis. Our findings suggest a comprehensive role of HGlyc as a structural and functional modulator of energy metabolism, and such roles may come into play relatively rapidly. [ABSTRACT FROM AUTHOR]

A trend in large yellow croaker (Larimichthys crocea) aquaculture is to establish production sites suitable for extreme weather conditions. However, continuous and strong currents can harm fish welfare. To determine a suitable site location, the swimming ability of large yellow croakers must be assessed. This study aims to provide novel insights into the physiological characteristics of large yellow croaker swimming and a reference for fishing and cage site selection. Currently, research on large yellow croakers has focused on behavior analysis. Herein, we investigate the effects of swimming on large yellow croakers’ metabolites by examining the preferred speed of the group and the sustained swimming ability of single-tailed fish. We evaluated factors that influence the large yellow croaker’s swimming fatigue by quantifying the metabolite contents and constructing a sustained swimming model. The results showed that large yellow croaker populations tend to grow in low-velocity environments, similar to their traditional habitat. The samples were taken at different swimming times at a flow velocity of 0.35 m/s. According to the results of the metabolite content analysis, blood glucose levels are closely associated with the swimming ability in large yellow croakers. The content of liver glycogen, which regulates blood glucose concentration, decreased in a certain linear relationship. The sustained swimming model of the large yellow croaker was constructed according to the changes in liver glycogen content. Based on our findings, we recommend the following: (1) for large yellow croakers with a size of approximately 13.5 cm (approximately 1 year old), the water velocity inside the cage should not exceed 2.6 BL/s; (2) the concentration of liver glycogen limits the sustained swimming ability of the large yellow croaker, providing a reference for studying the swimming ability of other fish.

Background/Aims: Glycogen synthesis and storage are normal hepatocyte functions. However, glycogenosis, defined as excess hepatocyte glycogen visible by routine H&E light microscopy, has not been well characterized in nonalcoholic fatty liver disease (NAFLD). Methods: Glycogenosis in NAFLD liver biopsies was graded as "none", "focal" (in <50% of hepatocytes), or "diffuse" (in ≥50% of hepatocytes). Clinical and pathological variables associated with glycogenosis were assessed. 2047 liver biopsies were prospectively analysed. Results: In adults and children, any glycogenosis was present in 54% of cases; diffuse glycogenosis was noted in approximately 1/3 of cases. On multiple logistic regression analysis, adults with glycogenosis tended to be older (P =.003), female (P =.04), have higher serum glucose (P =.01), and use insulin (P =.02). Adults tended to have lower steatosis scores (P =.006) and lower fibrosis stages (P =.005); however, unexpectedly, they also tended to have more hepatocyte injury including ballooning (P =.003). On multiple logistic regression analysis, paediatric patients with glycogenosis were more likely to be Hispanic (P =.03), have lower body weight (P =.002), elevated triglycerides (P =.001), and a higher fasting glucose (P =.007). Paediatric patients with glycogenosis also had less steatosis (P <.001) than those without. Conclusions: Glycogenosis is common in adult and paediatric NAFLD, and is associated with clinical features of insulin resistance. Glycogenosis is important to recognize histologically because it may be misinterpreted as ballooning, and when diffuse, confusion with glycogen storage disorders or glycogenic hepatopathy must be avoided. The newly observed dichotomous relationship between glycogenosis and increased liver cell injury but decreased steatosis and fibrosis requires further study. [ABSTRACT FROM AUTHOR]

Leptin affects food intake regulation and energy homeostasis in mammals, as opposed to mammals who have a single leptin gene, fish have duplicated leptin gene paralogues. Until now, most functional studies on fish focused on the first reported paralogue without much explanation on specific gene paralogue. This study successfully expressed two homologous recombinant mandarin fish leptin genes (LepA and LepB) for the first time. To explore the differential roles of these two gene paralogues involved in food intake and energy homeostasis, mandarin fish were treated with homologous recombinant LepA and LepB proteins by acute IP administration. The results showed that LepB inhibited the food intake of mandarin fish after acute IP administration through modifying the expressions of hypothalamic orexigenic genes, while LepA had no significant effect on its food intake. In addition, LepB administration decreased the hepatic glycogen level through regulating the gene expressions of glycogen synthase and glycogen phosphorylase in mandarin fish until 4 d, while LepA did not change the hepatic glycogen level as it failed to change the expressions of these regulatory genes. Moreover, LepA and LepB downregulated the expressions of key gluconeogenic genes (phosphofructokinase, phosphoenolpyruvate carboxykinase, and glucose-6-phosphatase), indicating both mandarin fish leptins could regulate the rate of glucose production. However, these two gene paralogues presented secondary effects on lipid metabolism as they only enhanced the triglyceride level by modifying the gene expressions of adipose triglyceride lipase or acetyl CoA carboxylase just for 1 d after IP. Therefore, LepB played an important role in food intake and glucose homeostasis regulation, while LepA showed a limited role in gluconeogenesis and lipid metabolism.

Practical diets for commercial barramundi production rarely contain greater than 10% starch, used mainly as a binding agent during extrusion. Alternative ingredients such as digestible starch have shown some capacity to spare dietary protein catabolism to generate glucose. In the present study, a carnivorous fish species, the Asian seabass (Lates calcarifer) was subjected to two diets with the same digestible energy: Protein (P) – with high protein content (no digestible starch); and Starch (S) – with high digestible (pregelatinized) starch content. The effects of a high starch content diet on hepatic glycogen synthesis as well as the muscle and liver metabolome were studied using a complementary approach of 1H and 2H NMR. The hepatosomatic index was lower for fish fed high starch content diet while the concentration of hepatic glycogen was similar between groups. However, increased glycogen synthesis via the direct pathway was observed in the fish fed high starch content diet which is indicative of increased carbohydrate utilization. Multivariate analysis also showed differences between groups in the metabolome of both tissues. Univariate analysis revealed more variations in liver than in muscle of fish fed high starch content diet. Variations in metabolome were generally in agreement with the increase in the glycogen synthesis through direct pathway, however, this metabolic shift seemed to be insufficient to keep the growth rate as ensured by the diet with high protein content. Although liver glycogen does not make up a substantial quantity of total stored dietary energy in carnivorous fish, it is a key regulatory intermediate in dietary energy utilization.

Leptin affects food intake regulation and energy homeostasis in mammals, as opposed to mammals who have a single leptin gene, fish have duplicated leptin gene paralogues. Until now, most functional studies on fish focused on the first reported paralogue without much explanation on specific gene paralogue. This study successfully expressed two homologous recombinant mandarin fish leptin genes (LepA and LepB) for the first time. To explore the differential roles of these two gene paralogues involved in food intake and energy homeostasis, mandarin fish were treated with homologous recombinant LepA and LepB proteins by acute IP administration. The results showed that LepB inhibited the food intake of mandarin fish after acute IP administration through modifying the expressions of hypothalamic orexigenic genes, while LepA had no significant effect on its food intake. In addition, LepB administration decreased the hepatic glycogen level through regulating the gene expressions of glycogen synthase and glycogen phosphorylase in mandarin fish until 4 d, while LepA did not change the hepatic glycogen level as it failed to change the expressions of these regulatory genes. Moreover, LepA and LepB downregulated the expressions of key gluconeogenic genes (phosphofructokinase, phosphoenolpyruvate carboxykinase, and glucose-6-phosphatase), indicating both mandarin fish leptins could regulate the rate of glucose production. However, these two gene paralogues presented secondary effects on lipid metabolism as they only enhanced the triglyceride level by modifying the gene expressions of adipose triglyceride lipase or acetyl CoA carboxylase just for 1 d after IP. Therefore, LepB played an important role in food intake and glucose homeostasis regulation, while LepA showed a limited role in gluconeogenesis and lipid metabolism. [ABSTRACT FROM AUTHOR]

Objective To observe the effects of Shijinmo herbal-pair formula on the liver glycogen content, and PI3K/AKT/GSK-3β signaling pathway in type 2 diabetic rats, and to explore its action mechanism in reducing the insulin resistance. Methods Six rats were randomly selected from 40 rats and given common diet, and the rest were given highfat/sugar diet combined with intraperitoneal injection of low-dose streptozotocin to establish type 2 diabetic models. Twentyfour diabetic rats were randomly divided into the model control group, and low-dose, medium-dose and high-dose Shijinmo herbal-pair formula groups, with 6 rats in each group. The rats in the normal control group and the model control group were given pure water ( 1. 5 mL/100 g), and the rats in the low-dose, medium-dose and high-dose Shijinmo herbal-pair formula groups were given the corresponding drugs (equals to the original herbs of 5. 8, 11. 6 and 23. 2 glkg) for 8 weeks. Blood glucose was measured with glucose oxidase method. The level of serum insulin was measured by ELISA. The HomaIR formula was used to calculate IR index. The hepatic glycogen content was measured by the glycogen assay kit; the protein expression levels of PI3K, AKT and GSK-3β, and their phosphorylation levels were analyzed by Western blotting. Results Compared with the normal control group, the blood glucose level increased, IRI increased, liver glycogen content decreased, the protein express levels of PI3 K and AKT, and their phosphorylation levels decreased, GSK-3β protein expression increased, but its phosphorylation level decreased in the model control group (all P < 0. 05) . Compared with the model control group, the blood glucose level and IRI value were significantly reduced, the glycogen content in the liver increased in type 2 diabetic rats after the treatment of low-dose Shijinmo herbal-pair formula group. The low-dose Shijinmo herbal-pair formula increased the protein expression levels of PI3K and AKT and their phosphorylation levels, and decreased the protein level of GSK-3β but enhanced its phosphorylation level (all P <0. 05). The above indicators were not significantly improved in the medium-dose and high-dose Shijinmo herbal-pair formula groups. Conclusion Shijinmo herbal-pair formula has hypoglycemic effect through enhancing the insulin signal transduction pathway of PBK-AKT-GSK3β, thereby increasing the glycogen content in hepatocytes and reducing the degree of IR. [ABSTRACT FROM AUTHOR]

Objective: The present study aimed to evaluate and clarify how the age at which the intake of a high-fat and high-fructose diet begins can affect animals' livers. Methods: Thirty-eight male wistar rats aged 6 and 12 weeks were fed a high-fat and high-fructose diet for 13 weeks. Inflammatory cytokines, hepatic glycogen, serum and hepatic triacylglycerol and pAkt protein content in the liver were assessed. Percentage of weight gained, and visceral adiposity were also evaluated. Results: Young animal presented increased hepatic triacylglycerol and decreased glycogen, while adult animals had no significant alterations regarding its contents. IL6 and IL10 to IL6 ratio were also altered in young animals exposed to HFHF, while adult animals fed with HFHF had only increases in TNF-α. Both groups which received HFHF had increased serum triacylglycerol and visceral adiposity. However, only young animals gained more relative weight and had greater final body weight, gains which were related to alterations found in hepatic triacylglycerol and glycogen. Conclusion: Age of which consumption begins interferes in how the liver deals with an excess of nutrient and subsequent proinflammatory stimulation, leading to different phenotypes. [ABSTRACT FROM AUTHOR]

Background: Our previous case series suggested that a 1-week, low-calorie and low-fat diet was associated with decreased intraoperative blood loss in patients undergoing liver surgery. Objective: The current study evaluates the effect of this diet in a randomized controlled trial. Methods: We randomly assigned 60 patients with a body mass index ≥25 kg/m2 to no special diet or an 800-kcal, 20 g fat, and 70 g protein diet for 1 week before liver resection. Surgeons were blinded to diet assignment. Hepatic glycogen stores were evaluated using periodic acid Schiff (PAS) stains. Results: Ninety four percent of the patients complied with the diet. The diet group consumed fewer daily total calories (807 vs 1968 kcal, P < 0.001) and fat (21 vs 86 g, P < 0.001) than the no diet group. Intraoperative blood loss was less in the diet group: mean blood loss 452 vs 863 mL (P = 0.021). There was a trend towards decreased transfusion in the diet group (138 vs 322 mL, P = 0.06). The surgeon judged the liver to be easier to manipulate in the diet group: 1.86 versus 2.90, P = 0.004. Complication rate (20% vs 17%), length of stay (median 5 vs 4 days) and mortality did not differ between groups. There was no difference in hepatic steatosis between groups. There was less glycogen in hepatocytes in the diet group (PAS stain score 1.61 vs 2.46, P < 0.0001). Conclusions: A short-course, low-fat, and low-calorie diet significantly decreases bleeding and makes the liver easier to manipulate in hepatic surgery. [ABSTRACT FROM AUTHOR]

Pharmaceutical drugs in the aquatic environment can induce adverse effects on nontarget organisms. This study aimed to assess the short-term effects of sublethal concentrations of both paracetamol and propranolol on the fish Phalloceros harpagos, specifically light/dark preference, swimming patterns, skin pigmentation, histopathology, and liver glycogen levels. Fish were acutely exposed to sublethal concentrations of both paracetamol (0.008, 0.08, 0.8, 8, 80 mg L−1) and propranolol (0.0001, 0.001, 0.01, 0.1, 1 mg L−1) under controlled conditions. For scototaxis, a significant preference for the dark compartment was observed for the group exposed to the highest concentration of paracetamol (80 mg L−1). Propranolol exposure significantly altered the swimming pattern, especially in fish exposed to the 0.001 mg L−1 concentration. Pigmentation was reduced in propranolol-exposed fish (0.1, 1 mg L−1). The lowest concentration of propranolol (0.0001 mg L−1) induced a decrease of histochemical reaction for hepatic glycogen. These data demonstrate that pharmaceuticals can induce sublethal effects in nontarget organisms, even at low concentrations, compromising specific functions of the individual with ecological relevance, such as energy balance and behavior. [ABSTRACT FROM AUTHOR]

OBJECTIVES: Ichnocarpus frutescens is a common plant used by tribal people and in Ayurveda for its high medicinal value. The purpose of the study was to investigate whether I. frutescens has any persuasive medicinal property to manage diabetes mellitus. MATERIALS AND METHODS: Initially, male albino Wistar rats were given intraperitoneal injection of streptozotocin-nicotinamide to induce diabetes, followed with the administration of active fraction obtained from the methanolic extract of I. frutescens for the next 28 consecutive days. Glibenclamide (25 mg/kg) was used as positive control. RESULTS: According to the results obtained, active fraction at a dose of 50 mg/kg body weight exhibited significant antihyperglycemic activity, which was evident with reduced blood glucose level up to 58.84%. The active fraction also showed improvement in serum lipid profile as well as regeneration of pancreatic β-cells in diabetic rats. Concurrent histopathological studies reinforce the effect of active fraction in healing pancreas, thus justifying the possible mechanism of its antidiabetic activity. CONCLUSION: The results of the present investigation lead credence to the use of I. frutescens in ameliorating the diabetic condition. [ABSTRACT FROM AUTHOR]

In this study, a particular pectic polysaccharide (FPLP) was extracted and purified from the fruits of Ficus pumila Linn. through boiling water extraction, alcohol precipitation, diethylaminoethyl-Sepharose Fast Flow chromatography and Superdex™ G-75 gel filtration chromatography. Analysis of high-performance gel permeation chromatography, FTIR, GC–MS, methylation and 1D/2D NMR spectroscopy revealed that FPLP (Mw: 34.69 kDa) is a linear (1,4)-α- d -galacturonic acid binding 1.30% branched chain hexenuronic acid with 23.34% methyl esterification. Treatment with FPLP ameliorated hyperglycaemia in association with an improvement in hepatic glycogen metabolism in C57BL/KsJ db/db mice. The activation of IRS-1/PI3K/Akt/GSK3β/GS insulin signalling pathway and AMPK/GSK3β/GS signalling pathway and the regulation of glucokinase, phosphoenolpyruvate carboxykinase and glucose-6-phosphatase expressions involved in hepatic glycogenesis and glycogenolysis were considered the therapeutic mechanisms of FPLP. These results provide a new insight for investigating the effects of pectic polysaccharides on blood glucose control and suggest that FPLP is a promising nutraceutical for treatment of T2DM. [ABSTRACT FROM AUTHOR]

Background: Diabetes is associated with both biochemical and haematological complications. Combination therapy has been advocated to mitigate some of these complications. Aim: This study was designed to investigate the effects of glibenclamide and Gongronema latifolium (GL) on hepatic glycogen content and haemato-biochemical parameters. Methods: Thirty male Wistar rats were assigned into five groups of six rats each. Groups 2-5 rats received intraperitoneally, 160 mg/kg of alloxan monohydrate while group 1 rats served as normal control. Groups 2-5 rats were respectively treated with 10 mL/kg distilled water (DW), 2 mg/kg glibenclamide, 200 mg/kg GL and 2 mg/kg glibenclamide and 200 mg/kg GL, while group 1 rats received 10 mL/kg DW. All treatments were per os daily for 21 days. Blood samples for investigation of haemato-biochemical (red blood cell [RBC], packed cell volume [PCV], haemoglobin concentration [Hb], blood urea nitrogen [BUN] and creatinine) parameters were collected on days 7, 14 and 21 post-treatment (PT), while the liver sample for hepatic glycogen determination was obtained on day 21 PT. Results: Creatinine and BUN values of groups 3 and 4 rats were comparable to that of group 1 but were significantly (p<0.05) lower when compared with those of groups 2 and 5. There were significant (p<0.05) increases in the mean hepatic glycogen content, RBC, PCV, and Hb of group 4 rats when compared to those of group 2. Conclusions: It was concluded that a combination of glibenclamide and G. latifolium in treatment of diabetic rats improved glycogen storage and demonstrated beneficial effects on haematology and kidney marker parameters. [ABSTRACT FROM AUTHOR]

Recent studies have shown that rambutan peel phenolic (RPP) extract demonstrate high antioxidant and antiglycation activities in vitro and in vivo. This study further evaluated the anti-diabetic activity of RPP in a mouse model of Type II diabetes induced by streptozotocin combined with high-fat diet. Results showed that RPP increased the body weight and reduced the fasting blood glucose level of the diabetic mice. RPP significantly reduced the serum levels of total cholesterol, triglyceride, creatinine, and glycated serum protein in diabetic mice in a dose-dependent manner. Glycogen content in mice liver was recovered by RPP, which further increased the activity of superoxide dismutase and glutathione peroxidase and reduced lipid peroxidation in diabetic mice. Histological analysis showed that RPP effectively protected the tissue structure of the liver, kidney, and pancreas. In addition, RPP decreased the mesangial index and inhibited the expression of TGF-β in the kidney of diabetic mice. [ABSTRACT FROM AUTHOR]

We investigated effects of eggshell temperature (EST) of 35.6, 36.7, 37.8, or 38.9°C applied from d of incubation (E) 15, E17, or E19 onward on chicken embryo physiology. A total of 2,850 first-grade eggs of a 43-week-old Ross 308 broiler breeder flock were incubated at an EST of 37.8°C until E15. From E15, E17, or E19 onward, eggs were incubated at an EST of 35.6, 36.7, 37.8, or 38.9°C. Plasma glucose, uric acid, and lactate concentrations, and hepatic glycogen amount and concentration were measured at E15, E17, E19, internal pipping (IP), external pipping (EP), and hatch. An EST of 38.9°C applied from E15 onward decreased the amount of hepatic glycogen from E19 to IP and resulted in a lower glycogen amount at IP compared to all other EST. At EP, when oxygen (O2) becomes largely available, an EST of 38.9°C resulted in a higher glycogen amount and concentration compared to IP, which suggests that plasma glucose between IP and EP might be used for building up hepatic glycogen reserves. However, hepatic glycogen levels remained considerably lower at IP, EP, and hatch at an EST of 38.9°C, compared to an EST of 35.6 and 36.7°C. Opposite to an EST of 38.9°C, from IP onward, an EST of 35.6°C resulted in a higher glycogen amount and concentration compared to all other EST, which might be caused by the higher O2 availability relative to the lower metabolic rate, which provided time to build up glycogen stores from excessive glucose. A higher availability of hepatic glycogen might contribute to an improved physiological status of the broiler chicken embryo toward hatch. Hepatic gluconeogenesis is crucial for developing embryos, as glucose is the major energy source from IP until hatch. At hatch, no effect of EST was found for glucose, uric acid, or lactate. Results of this study emphasize that EST of 35.6 and 36.7°C from E15 onward appear to be beneficial for chicken embryo physiology. [ABSTRACT FROM AUTHOR]

Previous studies have indicated that polyphenol-rich Chrysanthemum morifolium extract (CME) may inhibit the formation of hyperlipidemic fatty liver in mice. But there has been no report about therapeutic effect on diabetes mellitus. In the present study, we investigated the action of CME and its potential mechanisms. A mouse model with diabetes mellitus was induced by alloxan. The results showed that after treatment of diabetic mice with polyphenol-rich CME 150 and 300 mg/kg for 6 weeks, the levels of fasting blood glucose (FBG) as well as water and food consumption were decreased ( P < 0.05 or P < 0.01), the content of hepatic glycogen was increased, especially in the 300 mg/kg group ( P < 0.05), but no significant variations in the body-weight gain, fasting serum insulin, and muscular glycogen were observed. Importantly, toxic alloxan treatment might decrease the protein expressions of hepatic peroxisome proliferator-activated receptor (PPAR) α/γ, glycogen synthase (GS), and glucose transporter-2 (Glut-2) ( P < 0.05 or P < 0.01), while CME might reverse the changes ( P < 0.01). These findings demonstrate that the reduction of PPARα/γ-mediated hepatic glycogen synthesis may involve in the alloxan-induced hyperglycemia, and the hypoglycemic mechanisms of CME may be mainly associated with the increment of hepatic glycogen synthesis via upregulation of PPARα/γ-mediated GS and Glut-2 protein expressions. [ABSTRACT FROM AUTHOR]

Glycogen levels and the energy status of livers from fasting rats with diabetes types 1 and 2 were measured. After a 24 h fast, the hepatic glycogen levels of rats with diabetes1 and diabetes2 were, 18.7 and 2.6 times higher, respectively, than those of livers from the normal rats. In diabetes1 rats, the glycogen levels decreased when the fasting period was extended to 48 and 72 h. The opposite occurred with the control and diabetes2 rats. Consistently, glucose release by the perfused livers from diabetes1 rats was considerably higher during at least 60 minutes after initiating perfusion. The hepatic ATP content of diabetes1 rats was similar to that of the control rats; in diabetes2 rats, the hepatic ATP content was increased. It could be concluded that regulation of glycogen deposition and degradation in rats with diabetes1 differed markedly from that of rats with diabetes2 which, in turn, behaved similarly to normal healthy rats.Teores de glicogênio e os estados energéticos de fígados de ratos com diabete dos tipos 1 e 2 foram medidos. Após um jejum de 24 horas os teores de glicogênio de ratos com diabete1 e diabete2 foram, respectivamente 18,7 e 2,6 vezes superiores àqueles de fígados de animais controle. Em ratos com diabete1 o conteúdo de glicogênio diminuiu quando o período de jejum foi prolongado para 48 e 72 horas. O oposto ocorreu em ratos controle e ratos com diabete2. Consistentemente, a liberação de glicose por fígados em perfusão isolada obtidos de ratos com diabete1 foi consideravelmente maior durante ao menos 60 minutos após o início da perfusão. O conteúdo hepático de ATP de ratos com diabete1 foi similar àquele de ratos controle; em ratos com diabete2 o conteúdo hepático de ATP foi maior. Pode-se concluir que a regulação da deposição e degradação do glicogênio em ratos com diabete1 difere marcadamente daquela de ratos com diabete2, os quais, por seu turno, comportam-se similarmente a ratos normais e saudáveis.

Objective To investigate the effect against exercise-indused fatigue in mice by aqueous extract of Ludisia discolor and its mechanism. Methods Male mice were randomly divided into five groups including low, middle, high dose groups [aqueous extract of Ludisia discolor at dose of 1.22, 2.44, 4.88 g/(kg·d) respectively], positive control group [aqueous extract of Rhodiola, at dose of 2.34 g/(kg·d)] and control group (distilled water). After intragastric administration for seven days, mice were measured for loading swimming time, and were tested 90 minutes after loading swimming for blood urea nitrogen, blood lactic acid and hepatic glycogen levels. Results The blood urea nitrogen was significantly decreased (P<0.05) in aqueous extract of Ludisia discolor groups, and hepatic glycogen was significantly increased (P<0.05) in a dose-dependent manner. The blood lactic acid was significantly decreased in high dose group, and weight loading swimming time was prolonged (P<0.05). The effects of Ludisia discolor is similar compared to Rhodiola. Conclusion The aqueous extract of Ludisia discolor has anti-fatigue action in mice. The mechanism might be related with the increased glycogen reserves, increased glucose aerobic decomposition, as well as reduced anaerobic glucolysis and reduced protein breakdown. [ABSTRACT FROM AUTHOR]

An acute bout of exercise elicits a rapid, potentially deleterious, reduction in blood glucose in patients with type 1 diabetes mellitus (T1DM). In the current study, we examined whether a 10-week aerobic training program could alleviate the rapid exercise-associated reduction in blood glucose through changes in the glucoregulatory hormonal response or increased hepatic glycogen storage in an insulin-treated rat model of T1DM. Thirty-two male Sprague-Dawley rats were divided evenly into 4 groups: non-T1DM sedentary (C) ( n = 8), non-T1DM exercised (CX) ( n = 8), T1DM sedentary (D) ( n = 8), and T1DM exercised (DX) ( n = 8). Exercise training consisted of treadmill running for 5 days/week (1 h, 27 m/min, 6% grade) for 10 weeks. T1DM was induced by multiple streptozotocin injections (20 mg/kg) followed by implantation of subcutaneous insulin pellets. At week 1, an acute exercise bout led to a significant reduction in blood glucose in DX ( p < 0.05), whereas CX exhibited an increase in blood glucose ( p < 0.05). During acute exercise, serum epinephrine was increased in both DX and CX ( p < 0.05), whereas serum glucagon was increased during recovery only in CX ( p < 0.01). Following aerobic training in DX, the exercise-mediated reduction in blood glucose remained; however, serum glucagon increased to the same extent as in CX ( p < 0.05). DX exhibited significantly less hepatic glycogen ( p < 0.001) despite elevations in glycogenic proteins in the liver ( p < 0.05). Elevated serum epinephrine and decreased hepatic adrenergic receptor expression were also evident in DX ( p < 0.05). In summary, despite aerobic training in DX, abrupt blood glucose reductions and hepatic glycogen deficiencies were evident. These data suggest that sympathetic overactivity may contribute to deficiencies in hepatic glycogen storage. [ABSTRACT FROM AUTHOR]

The present study investigated the effect of 1-Deoxynojirimycin (DNJ) on liver injury and hepatic glucose metabolism in db/db mice. Mice were divided into five groups: normal control, db/db control, DNJ-20 (DNJ 20 mg. kg-1. day-1), DNJ-40 (DNJ 40 mg-1 kg-1. day-1) and DNJ-80 (DNJ 80 mg. kg-1. day-1). All doses were treated intravenously by tail vein for four weeks. DNJ was observed to significantly reduce the levels of serum triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and liver TG, as well as activities of serum alanine aminotransferase (ALT), and aspartate transaminase (AST); DNJ also alleviated macrovesicular steatosis and decreased tumor necrosis factor α (TNF-α), interleukin-1 (IL-1), interleukin-6 (IL-6) levels in liver tissue. Furthermore, DNJ treatment significantly increased hepatic glycogen content, the activities of hexokinase (HK), pyruvate kinase (PK) in liver tissue, and decreased the activities of glucose-6-phosphatase (G6Pase), glycogen phosphorylase (GP), and phosphoenolpyruvate carboxykinase (PEPCK). Moreover, DNJ increased the phosphorylation of phosphatidylinositol 3 kinase (PI3K) on p85, protein kinase B (PKB) on Ser473, glycogen synthase kinase 3β (GSK-3β) on Ser9, and inhibited phosphorylation of glycogen synthase (GS) on Ser645 in liver tissue of db/db mice. These results demonstrate that DNJ can increase hepatic insulin sensitivity via strengthening of the insulin-stimulated PKB/GSK-3β signal pathway and by modulating glucose metabolic enzymes in db/db mice. Moreover, DNJ also can improve lipid homeostasis and attenuate hepatic steatosis in db/db mice. [ABSTRACT FROM AUTHOR]

BACKGROUND: Glutamine has been widely used in treatment of small bowel syndrome and its metabolic effects on the small intestine are well known, however, it has been little studied its effects on hepatic metabolism under this condition. AIM: To verify through experimental model, a glutamine based supplemental diet, administered via oral to rats submitted to massive intestinal resection, evaluating weight evolution and hepatic glycogen content. MATERIAL AND METHODS: Male rats, Wistar, were allocated into three groups to undergo enterectomy. Following diets were applied: with glutamine (G group), without glutamine (NG group), and standard diet from the laboratory (R group). All animals had massive small intestine resection including ileocecal valve removal. After 20 days, all animals were sacrificed. The liver was removed to histological analysis by light microscopy. Slides were stained by periodic acid of Schiff with diastasis. RESULTS: All animals lost weight from the beginning to the end of experiment. Comparing weight loss average expressed in percentage, there was no difference statistically significant on this variance. In analyzed groups, the hepatic glycogen content did not differ statistically, in the histological method evaluated. CONCLUSION: Glutamine feeding via oral did not influence weight loss reduction of animal submitted to massive intestinal resection and did not stimulate glycogen synthesis and storage into hepatocytes.RACIONAL: A glutamina tem sido utilizada amplamente no tratamento da síndrome do intestino curto e seus efeitos metabólicos são bem conhecidos no intestino delgado, porém pouco se tem relatado sobre seus efeitos no metabolismo hepático nessa condição. OBJETIVO: Verificar em modelo experimental, o efeito de dieta suplementada com glutamina administrada por via oral, em ratos submetidos a ressecção intestinal extensa, na evolução ponderal e no conteúdo de glicogênio hepático. MATERIAL E MÉTODOS: Ratos Wistar machos foram distribuídos em três grupos enterectomizados. As seguintes dietas foram utilizadas: com glutamina (grupo G), sem glutamina (grupo NG) e a dieta padrão do laboratório (grupo R). Em todos os animais a ressecção extensa do intestino delgado incluiu a válvula íleo-cecal. Após 20 dias os animais foram sacrificados. O fígado foi retirado para estudo histológico por microscopia ótica. As lâminas foram coradas pelo ácido periódico com base de Schiff com diastase. RESULTADOS: Todos os animais perderam peso entre o inicio e o final da pesquisa. Na comparação da perda média de peso expressa em percentagem, não houve diferença estatística em relação a essa variável. Nos grupos estudados o conteúdo de glicogênio no hepatócito, avaliado por método histológico, não diferiu estatisticamente. CONCLUSÕES: A oferta de glutamina por via oral não contribuiu para redução da perda de peso dos animais submetidos a ressecção intestinal extensa e não estimulou a síntese e armazenamento de glicogênio nos hepatócitos.

Livers cold preserved during variable periods of ischemia suffer functional, morphological and hemodynamic alteration, which are exacerbated when they are reperfused. One important injury is glycogen depletion during cold ischemia/ reperfusion. How liver can restore their energy during reperfusion is related with the preservation time, nutritional status of the donor, and the preservation solution used. However, there are some treatments that help livers to preserve their energy storage. These procedures used drugs or metabolites, which are added to the liver to maintain their glycogen storage during preservation, time and allow the organ to restore its energy during reperfusion. There are several publications where the nutritional status of the donor was studied. There is controversy about the quality or the donor organ. Some authors say that fasted animals are better donors because this condition reduced hepatic injuries; others think that fed animals provide the necessary glycogen (energy) to improve liver preservation, reducing morphological and functional damages. Many others are convinced that nutritional status of the donor is not relevant because hepatic injuries will occurred even though the donor was fed or not. The preservation solution has an important role in reducing liver damages during cold ischemia/reperfusion and in restoring liver energy storage. Storage in HLR (histidine, lactobionate and raffinose) solution facilitated the resuscitation of energetic status and preserved adenine nucleotide levels significantly greater than Marshall’s citrate or Bretschneider’s histidine-based solution (HTK). University of Wisconsin (UW) proved to be suitable for energy recovery during reperfusion. In conclusion, the aim of this review is to present studies performed by different authors where they analyzed preservation/reperfusion injuries, how the liver restores its energy storage during reperfusion time, different strategies to avoid glycogen depletion during cold ischemia/reperfusion, the efficacy of preservation solutions and the effect of nutritional status of the donor to prevent functional alteration of the liver during cold preservation.

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Cordyceps militaris has long been used in prescriptions of traditional Chinese medicine as a tonic for the treatment of metabolic syndrome. Cordycepin with proven immunomodulatory, antitumor, and hepatoprotective properties is the main active metabolite of C militaris . Diabetes mellitus is a group of metabolic diseases in which the body is unable to regulate blood sugar levels. Hence, we hypothesized that cordycepin can normalize blood sugar levels and improve the indicators of diabetes. The aim of this study was to investigate the possible effects of cordycepin from C militaris on diabetes in an alloxan-induced diabetic mouse model. Diabetic mice were intraperitoneally administered different doses of cordycepin (8, 24, and 72 mg/kg body weight) daily for 21 days. Acute toxicity test on normal mice was carried out by giving them maximum tolerance dose of cordycepin (3600 mg/kg) daily. A 47% reduction of the blood glucose level, 214% increase of hepatic glycogen content, and significant improvement of oral glucose tolerance were noticed after the effective dose of cordycepin was administered. Polyphagia and polydipsia, the typical symptoms of diabetes, were partly alleviated. Moreover, cordycepin offered protective effects against diabetes-related kidney and spleen injury. Maximum tolerance dose test indicated that cordycepin at the large dose of 3600 mg/kg did not show significant effect on body weight and major organ in normal mice after intraperitoneal administration for 14 days. The results showed that cordycepin from C militaris that elicited hypoglycemic activity contributes to the regulation of glucose metabolism in liver in alloxan-induced diabetic mice. Therefore, a cordycepin treatment during diabetes can improve some of the metabolic syndrome symptoms by regulation of glucose absorption in vivo. Cordycepin may serve as a therapeutic agent in the treatment of diabetes and its related complications. [ABSTRACT FROM AUTHOR]

Background: Growth hormone (GH) is a peptide hormone that plays vital roles in cell growth and metabolism. Aim: The study investigates the effect of GH on carbohydrate metabolism using Indian bird, Acridotheres tristis. Methods: Three different doses (0.4, 0.6, and 0.8mg/100g body weight) of human growth hormone (HGH) given once to both genders of a bird Acridotheres tristis to observe the effect on blood glucose and hepatic glycogen content in the body. Glucose and glycogen were quantitatively assayed. Results: Their effect was recorded for different time intervals (1, 4, 12, 24, 72, 96, and 144 h). Hypoglycaemic condition was recorded within an hour of hormone treatment in male and female birds. The lowest dose (0.4mg/100g body weight) was more effective than other two doses. Simultaneous depletion of hepatic glycogen was also recorded, although initially increase in glycogen level was also noticed in both genders. It was noticed that the highest dose (0.8mg/100g body weight) was most responsive. Conclusion: The effect of human growth hormone was not dose and time dependent in both male and female birds. HGH is thus hypoglycaemic and hepatic glycogenolytic in nature in A. tristis. [ABSTRACT FROM AUTHOR]

The current paper aimed to study the influence of artificial rearing conditions on glycogen quantity for two trout breeds - rainbow trout (Oncorhynchus mykiss - Walbaum, 1792) and brook trout (Salvelinus fontinalis - Richardson, 1836), analysing 40 individuals, 20 individuals from each breed, belonging to Cheiţa trout farm from Neamţ County. The current research is a part of an ample study designed to enlighten the differences of nutritional value for human consumption of trout meat reared in natural and artificial conditions. Trout represent also an important source of carbohydrates, through its reserves of hepatic and muscular glycogen. Glycogen is synthesised in animal organism by the mono-carbohydrates supplied by food, and in the case of an insufficient contribution of alimentary carbohydrates, it is formed from the resulted products of lipids and proteins catabolism. The obtained data resulted at the end of effectuated analysis on hepatic tissue record mean values of 2.325±0.892 g/100g for rainbow trout and of 3.832±0.450 g/100g for brook trout. In the case of muscular tissue were recorded mean values of 0.098±0.016 g/100g for rainbow trout and 0.130±0.044 g/100g for brook trout. Non-uniformity of biological material as regarding the corporal development and implicit of the tracked carbohydrates parameters have a great influence on the results, increasing in a considerable way their variability degree. [ABSTRACT FROM AUTHOR]

It was in Saint-Julien near Villefranche that Claude Bernard was born on 12 July 1813. About 20 years later he moved to Paris to become a dramatist but was directed into the study of medicine, the service at the Hôtel Dieu of Magendie that led him to the Collège de France. He entered Magendie's laboratory as a voluntary assistant and within a year became official préparateur. His early work on the chorda tympani and his MD thesis on gastric juice in 1843 set him on his lifelong discoveries in physiology. The central role of hepatic glycogenesis in the formation of sugar in animals was established around 1850, and he proceeded to show that section of the cervical fibres of the sympathetic chain led to congestion and increased temperature on that side of the face-resulting from paralysis of the vasomotor nerves. And there were vasodilator as well as vasoconstrictor fibres. After the salivary glands, the pancreas caught his attention and he discovered its ability to emulsify fatty material. Toxic and therapeutic substances were analysed: carbon monoxide paralyses carriage of oxygen by taking its place on haemoglobin; and curare abolishes voluntary movement by paralysis at the motor end-plate. But Bernard was above all a general physiologist, exemplified in 1872 and 1873 in his Lectures on the phenomena of life common to animals and plants, summarised in the aperçu 'the constancy of the internal environment is the condition of the free and independent life'. Claude Bernard died on Sunday 10 February 1878 in Paris. [ABSTRACT FROM AUTHOR]