scholarly journals Starvation and feeding with a high-carbohydrate diet induce changes in the specific activity of rat hepatic pyruvate kinase

1985 ◽  
Vol 226 (1) ◽  
pp. 299-303 ◽  
Author(s):  
M A Cimbala ◽  
D Lau ◽  
J F Daigneault
Keyword(s):  
Catalytic Activity ◽  
Pyruvate Kinase ◽  
Opposite Effect ◽  
Specific Activity ◽  
High Carbohydrate Diet ◽  
Carbohydrate Diet ◽  
Immunoreactive Protein ◽  
High Carbohydrate

A highly specific radiosandwich assay for hepatic type-L pyruvate kinase (PK) determinants was developed. This assay was used to evaluate changes in PK specific activity which occur on starvation or feeding with a high-carbohydrate diet. Despite a large increase in both catalytic activity and immunoreactive protein, the calculated specific activity falls on feeding, and the opposite effect occurs on starvation. These change can be attributed to disproportionate changes in immunoreactive protein compared with changes in catalytic activity.

scholarly journals Studies on the biosynthesis of hepatic pyruvate kinase and its correlation with enhanced hepatic lipogenesis in meal-trained rats

1979 ◽  
Vol 182 (2) ◽  
pp. 383-397 ◽  
Author(s):  
T J Hopkirk ◽  
D P Bloxham
Keyword(s):  
Fatty Acid ◽  
Pyruvate Kinase ◽  
Fatty Acid Synthesis ◽  
Specific Activity ◽  
Acid Synthesis ◽  
High Carbohydrate Diet ◽  
Hill Coefficient ◽  
Carbohydrate Diet ◽  
High Carbohydrate ◽  
Maximum Activation

Metabolic and enzymic changes were measured in meal-trained rats fed on high-carbohydrate diet. Rates of hepatic fatty acid synthesis are probably greater than rates of gluconeogenesis throughout the 24 h day provided that animals are fed. The daily enhancement of fatty acid synthesis on meal feeding coincided with the maximum activation of hepatic pyruvate kinase. Maximum activation of this enzyme was reflected in increased total catalytic activity (Vmax.), increased activity at 0.5 MM-phosphoenolpyruvate (V0.5), decreased Vmax./V0.5 ratio and a decrease in co-operativity of phosphoenolpyruvate binding as measured by the Hill coefficient (h). The latter changes are consistent with a decrease in enzyme phosphorylation during activation of the enzyme. To estimate changes in enzyme protein, quantitative enzyme precipitation with rabbit antisera was used. Giving a high-carbohydrate diet to meal-trained animals induced enzyme synthesis within a few hours. Adaptations in diet that enhanced fatty acid synthesis (chow to high carbohydrate; starved to high carbohydrate) led to an increased steady-state concentration of pyruvate kinase protein. An approximate estimate of the half-life of hepatic pyruvate kinase was 56 h. Whenever pyruvate kinase specific activity was measured in liver tissue extracts it was always considerably less (20–100 mumol/min per mg of protein, depending on dietary status) than the specific activity of pure pyruvate kinase (200 mumol/min per mg of protein). Antigenically active, catalytically inactive protein was removed during enzyme purification from cytosol at the stage of (NH4)2SO4 fractionation. The fraction precipitated by 30–45%-satd. (NH4)2SO4 was enzymically active, antigenically reacting protein was identified in the remaining (NH4)2SO4 fractions (0–30%- and 45–85%-satd.) and this contained no enzyme activity. These may correspond to inactive proteolytic fragments of pyruvate kinase. The rate-determining step in adjusting enzyme concentration seems to be proteolysis.

scholarly journals Control in vivo of rat liver phosphofructokinase by glucagon and nutritional changes

1980 ◽  
Vol 186 (3) ◽  
pp. 953-957 ◽  
Author(s):  
A Nieto ◽  
J G Castaño
Keyword(s):  
Enzyme Activity ◽  
Pyruvate Kinase ◽  
High Protein Diet ◽  
High Carbohydrate Diet ◽  
Physiological Changes ◽  
Carbohydrate Diet ◽  
High Carbohydrate ◽  
Dietary Condition ◽  
Phosphofructokinase Activity

Glucagon (250 microgram/kg body wt.) intravenously injected into normal fed rats produces within 5 min a marked inactivation of liver phosphofructokinase, only observed when the enzyme activity is measured at subsaturating concentrations of fructose 6-phosphate. Since half-maximal inactivation is observed at a dose of glucagon of 0.32 microgram/body wt., a dose within the range of the physiological concentrations of the hormone, the inactivation of phosphofructokinase can occur in vivo in response to physiological changes in the concentration of glucagon. In gluconeogenic conditions (starved rats or high-protein-diet-fed rats), there is a marked inactivation of liver phosphofructokinase at subsaturating concentrations of fructose 6-phosphate similar to that found in normal fed rats after glucagon treatment. In these gluconeogenic conditions a 50% decrease in the Vmax. of the enzyme is also observed. No significant changes in phosphofructokinase activity either at subsaturating concentrations of fructose 6-phosphate or in the Vmax. of the enzyme are observed when rats are fed on a high-carbohydrate diet. In the last dietary condition, glucagon treatment produces similar effects to that described in the normal fed rats. Similar results have been obtained in the above condtions for pyruvate kinase L activity when measured at subsaturating concentrations of phosphoenolpyruvate.

scholarly journals The induction of synthesis of L-type pyruvate kinase in cultured rat hepatocytes

1982 ◽  
Vol 204 (1) ◽  
pp. 81-87 ◽  
Author(s):  
G P Poole ◽  
A D Postle ◽  
D P Bloxham
Keyword(s):  
Pyruvate Kinase ◽  
Rat Hepatocytes ◽  
Enzyme Synthesis ◽  
High Carbohydrate Diet ◽  
Lag Phase ◽  
Carbohydrate Diet ◽  
Adult Rats ◽  
High Carbohydrate ◽  
Culture Cells ◽  
Primary Monolayer

Hepatocytes were isolated from preweaned neonatal and adult rats and maintained in primary monolayer culture. Cells from preweaned newborns possessed no L-type pyruvate kinase, nor did they synthesize the enzyme. Incubation for 48-72 h in culture medium supplemented with 2 mM-fructose and 0.1 microM-insulin induced the synthesis of L-type pyruvate kinase, as judged by increased enzyme activity and the increased incorporation of [3H]leucine into immunoprecipitable L-type pyruvate kinase. Hepatocytes isolated from 48 h-starved adult rats incorporated less [3H]leucine into L-type pyruvate kinase than did cells isolated from high-carbohydrate-diet-fed rats. The rate of enzyme synthesis by cells from 48 h-starved rats was increased by the inclusion of fructose and insulin in the incubation medium, after a lag phase of 24-48 h. After 4 days in culture in the presence of fructose and insulin, hepatocytes from 48 h-starved rats synthesized L-type pyruvate kinase at similar rates to hepatocytes isolated from high-carbohydrate-diet-fed rats.

Regulation of blood glucose concentration: hepatic action of insulin

1961 ◽  
Vol 201 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Jack R. Leonards ◽  
Bernard R. Landau ◽  
James W. Craig ◽  
F. I. R. Martin ◽  
M. Miller ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Specific Activity ◽  
Blood Glucose Concentration ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
High Carbohydrate Diet ◽  
Carbohydrate Diet ◽  
High Carbohydrate ◽  
Hepatic Glucose ◽  
Glucose Output

Insulin was administered intravenously with or without the concurrent infusion of glucose to dogs surgically prepared so that hepatic glucose production could be measured directly. In dogs fed a high protein diet, hepatic glucose output as directly measured did not significantly change on insulin administration. The threshold at which a net hepatic glucose uptake occurred on the administration of a glucose load was unaffected by the presence of insulin. In contrast, in dogs fed a high carbohydrate diet, on the simultaneous infusion of insulin and glucose, a net uptake of glucose by the liver occurred at lower than normal plasma glucose concentrations. Hepatic glucose production was also estimated indirectly by isotopic techniques. A brief decrease in the rate of decline of plasma glucose specific activity was observed following the injection of C14-labeled glucose and then insulin in both protein and carbohydrate-fed animals. The explanation for this phenomenon remains uncertain. It is concluded that dietary status is important in determining the action of insulin on the liver. In dogs fed a high carbohydrate diet an almost immediate and perhaps direct action of insulin on the liver appears demonstrable.

scholarly journals High Carbohydrate Diet Increased Glucose Transporter Protein Levels in Jejunum but Did Not Lead to Enhanced Post-Exercise Skeletal Muscle Glycogen Recovery

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2140
Author(s):  
Yumiko Takahashi ◽  
Yutaka Matsunaga ◽  
Hiroki Yoshida ◽  
Terunaga Shinya ◽  
Ryo Sakaguchi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transporter ◽  
High Carbohydrate Diet ◽  
Oral Glucose ◽  
Carbohydrate Diet ◽  
Post Exercise ◽  
Glucose Administration ◽  
Protein Levels ◽  
High Carbohydrate ◽  
Glucose Transporter 2

We examined the effect of dietary carbohydrate intake on post-exercise glycogen recovery. Male Institute of Cancer Research (ICR) mice were fed moderate-carbohydrate chow (MCHO, 50%cal from carbohydrate) or high-carbohydrate chow (HCHO, 70%cal from carbohydrate) for 10 days. They then ran on a treadmill at 25 m/min for 60 min and administered an oral glucose solution (1.5 mg/g body weight). Compared to the MCHO group, the HCHO group showed significantly higher sodium-D-glucose co-transporter 1 protein levels in the brush border membrane fraction (p = 0.003) and the glucose transporter 2 level in the mucosa of jejunum (p = 0.004). At 30 min after the post-exercise glucose administration, the skeletal muscle and liver glycogen levels were not significantly different between the two diet groups. The blood glucose concentration from the portal vein (which is the entry site of nutrients from the gastrointestinal tract) was not significantly different between the groups at 15 min after the post-exercise glucose administration. There was no difference in the total or phosphorylated states of proteins related to glucose uptake and glycogen synthesis in skeletal muscle. Although the high-carbohydrate diet significantly increased glucose transporters in the jejunum, this adaptation stimulated neither glycogen recovery nor glucose absorption after the ingestion of post-exercise glucose.

scholarly journals Improvement of Obesity and Dyslipidemic Activity of Amomum tsao-ko in C57BL/6 Mice Fed a High-Carbohydrate Diet

Molecules ◽  
2021 ◽  
Vol 26 (6) ◽  
pp. 1638
Author(s):  
Ju-Hyoung Park ◽  
Eun-Kyung Ahn ◽  
Min Hee Hwang ◽  
Young Jin Park ◽  
Young-Rak Cho ◽  
...  
Keyword(s):  
Body Weight Gain ◽  
Subcutaneous Fat ◽  
Density Lipoprotein ◽  
Ethanol Extract ◽  
Cardiac Risk ◽  
Normal Diet ◽  
High Carbohydrate Diet ◽  
Atherogenic Index ◽  
Carbohydrate Diet ◽  
High Carbohydrate

Amomum tsao-ko Crevost et Lemaire (Zingiberaceae) is a medicinal herb found in Southeast Asia that is used for the treatment of malaria, abdominal pain, dyspepsia, etc. The aim of this study was to investigate the effect of an ethanol extract of Amomum tsao-ko (EAT) on obesity and hyperlipidemia in C57BL/6 mice fed a high-carbohydrate diet (HCD). First, the mice were divided into five groups (n = 6/group) as follows: normal diet, HCD, and HCD+EAT (100, 200, and 400 mg/kg/day), which were orally administered with EAT daily for 84 days. Using microcomputed tomography (micro-CT) analysis, we found that EAT inhibited not only body-weight gain, but also visceral fat and subcutaneous fat accumulation. Histological analysis confirmed that EAT decreased the size of fat tissues. EAT consistently improved various indices, including plasma levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein, high-density lipoprotein, atherogenic index, and cardiac risk factors, which are related to dyslipidemia—a major risk factor for heart disease. The contents of TC and TG, as well as the lipid droplets of HCD-induced hepatic accumulation in the liver tissue, were suppressed by EAT. Taken together, these findings suggest the possibility of developing EAT as a therapeutic agent for improving HCD-induced obesity and hyperlipidemia.

scholarly journals Mixed lineage kinase 3 deficient mice are protected against the high fat high carbohydrate diet-induced steatohepatitis

2013 ◽  
Vol 34 (3) ◽  
pp. 427-437 ◽  
Author(s):  
Samar H. Ibrahim ◽  
Gregory J. Gores ◽  
Petra Hirsova ◽  
Michelle Kirby ◽  
Lili Miles ◽  
...  
Keyword(s):  
High Carbohydrate Diet ◽  
High Fat ◽  
Carbohydrate Diet ◽  
Mixed Lineage Kinase ◽  
High Carbohydrate ◽  
Mixed Lineage Kinase 3 ◽  
Deficient Mice
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