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Objective: To observe the effect of puerarin on phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt) and glycogen synthase kinase-3β (GSK-3β) in insulin resistant HepG2 cells. Method: HepG2 cells were treated with palmitic acid 0.5 mmol·L-1 and insulin 9×10-4 U·L-1 to induce insulin resistant condition for 24 h. Cell viability was detected by methyl thiazolyl tetrazolium (MTT) assay to determine the concentration of puerarin. This experiment included normal control group, model control group and puerarin groups of different doses (40, 80, 160,320 μg·L-1). Glucose detection kit was used to detect the content of glucose in cell culture supernatant. Tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) levels in supernatant of cell culture medium were detected by enzyme-linked immunosorbent assay (ELISA). Hepatic glycogen assay kit was used for detecting the hepatic glycogen content in HepG2 cells. Western blot was applied to detect protein expression levels of PI3K, Akt, p-Akt, GSK-3β and p-GSK-3β. Result: Compared with those in the normal control group, the glucose consumption rate was significantly down-regulated in HepG2 cells in the model control group (PPα and IL-6 were increased in supernatant of cell culture medium (PPβ protein expression was up-regulated (PPα and IL-6 were reduced in supernatant of cell culture medium (PPβ protein expression was down-regulated, but its phosphorylation inactivation was increased (PConclusion: Puerarin alleviates the insulin resistance of HepG2 cells by strengthening the PI3K/Akt/GSK-3β signal transduction process and increasing the glycogen content in hepatocytes.
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Abstract Hepatic glycogen storage diseases (GSDs) are genetic diseases associated with fasting hypoglycemia. Periodic intake of uncooked cornstarch is one of the treatment strategies available for those disorders. For reasons that are still not clear, patients with hepatic GSDs may be overweight. Aims: To assess nutritional status and body composition in patients with hepatic GSDs receiving uncooked cornstarch. Methods: The sample included 25 patients with hepatic GSD (type Ia = 14; Ib = 6; III = 3; IX? = 1; IX? = 1), with a median age of 11.0 years (interquartile range [IQR] = 9.0-17.5), matched by age and gender with 25 healthy controls (median age = 12.0 years, IQR = 10.0-17.5). Clinical, biochemical, and treatment-related variables were obtained from medical records. Nutritional status and body composition were prospectively evaluated by bioelectrical impedance. Results: Patients and controls did not differ with regard to age and gender. Height was significantly reduced in patients (median = 1.43 m, IQR = 1.25-1.54) in comparison to controls (median = 1.54 m, IQR = 1.42-1.61; P = .04). Body mass index for age z-score and fat mass percentage were higher in patients (median = 1.84, IQR = 0.55-3.06; and 27.5%, IQR = 22.6-32.0, respectively) than in controls (median = 0.86, IQR = ?0.55 to 1.82; P = .04 and 21.1%, IQR = 13.0-28.3; P = .01, respectively). When patients were stratified by type, those with GSD Ia had significantly higher adiposity (median fat mass = 28.7%, IQR = 25.3-32.9) than those with GSD III and GSD IX?/? (median fat mass = 20.9%, IQR = 14.9-22.6; P = .02). Conclusions: Our findings suggest that patients with hepatic GSD on treatment with cornstarch, especially those with GSD Ia, exhibit abnormalities in nutritional status and body composition, such as short stature and a trend toward overweight and obesity.
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Objective To investigate the effect against exercise-indused fatigue in mice by aqueous extract of Ludisia dis-color 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 ex-tract 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 nitro-gen ,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 dis-color 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 .
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Objective To investigate the anti-fatigue effect of complex bear gall agent in mice.Methods Different dose of complex bear gall agent(4.4ml/kg、6.6ml/kg、13.2rml/kg)were given to mice by intragastric administration. The time of climbing-pole and loaded-swimming, hepatic glycogen content, serum urea nitrogen,lactic acid and lactate dehydrogenase of mice after swim were observed. Results The experiments indicated that complex bear gall agent could greatly increase the time of loaded-swimming and climbing Pole,increase the hepatic glycogen content and serum lactate dehydrogenase activity ,decrease serum urea nitrogen and blood lactic acid content in mice. Conclusion Complex bear gall agent had a significant anti-fatigue effect.
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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.
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Rats , Diabetes Mellitus, Type 1 , Glycogen , Liver , Perfusion , RatsABSTRACT
Objective To study renal involvement in hepatic glycogen storage disease(GSD) in childhood. Methods One hundred and eight patients aged less than 21 years old with type Ⅰa GSD (54 cases), type Ⅲ (29 cases) and uncertain type hepatic GSD (25 cases). Urine analysis, urine albumin, urine protein of 24 h, urine ?_2-MG, BUN, creatinine, Ccr were evaluated. Results Of 108 patients with hepatic GSD, 16 patients (20.8%) had proteinuria proven by urine albumin or urine protein of 24 h, their ages first found proteinuria were 8～15 years. Two 15-year-old patients had proteinuria over 1.0g/24h. Among 72 patients, urine ?_2-MG of 51 cases (70.8%) increased (175～10 623mg/L), and the mean urine ?_2-MG of type Ⅰ a GSD was much higher than that of type Ⅲ GSD, 4138.2 and 1790.1mg/L respectively. Of 91 patients, 10 had renal insufficiency, 1/10 (15-year-old girl) had heavy proteinuria (3.5g/24h), elevated BUN (9.3mmol/L) and Scr(1061 ?mol/L). Five elder patients (11～21 years old) had hematuria with renal colic caused by renal calculus. Conclusions Persistent protenuria, increased urine ?_2-MG, decreased Ccr, and renal stones are common complications of hepatic GSD in childhood. Renal function should be thoroughly evaluated during follow-up.
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The pectin isolated from the juice of the inflorescence stalk of plantain (Musa sapientum) has been found to show significant hypoglycemic effect both in normoglycemic and alloxan diabetic rats. After its administration at a dose of 20mg/100g body weight, there was increase in the concentration of hepatic glycogen, increased glycogenesis as evident from the increased activity of glycogen synthetase and in normoglycemic rats increased incorporation of labelled glucose into hepatic glycogen. Glycogenolysis and glyconeogenesis were lower as was evident from the decreased activity of glycogen phosphorylase and gluconeogenic enzymes.
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0. 05). Conclusion :Cordyceps sinensis can inhibit the hepatic fibrosis,and at the same time,doesn't improve the hepatic glycogen synthesis.
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A study was made; of the effect of malotilate on the acute liver injury induced by carbon tetrachlorid,e ( CC14 ) and d-galactosamine in mice. Malotilate ( 50~150mg/kg ig?3 ) significantly inhibited the elevation of serum glu tamic pyruvic transaminase ( SGPT ) in CC14- intoxicated mice.At the dose of 100mg/kg ig?3, malotilate remarkably increased the content of hepatic glycogea in CCl4-injected mice. The contents of serum protein, liver protein, and cytochrom P-450 in liver hemogenate were increased by malotilate ( 100mg/kg ig?3) in CC14-intoxicated mice. The drug also reduced the accumulation of liver triglycerides induced by CCl4 in mice.In addition to, malotilate(50mg /kg, ip?5) could act against the increase of SGPT and the decrease of liver protein content induced with d-galactosamine in mice. These results suggest that malotilate may be a new therapeutic agent for liver injury.