Time-course of changes of liver tryptophan pyrrolase (tryptophan oxygenase) and liver and kidney glucose-6-phosphatase in rats shifted from high- to zero-protein diets

Time-courses of changes in the activities of liver and kidney glucose-6-phosphatase [EC 3.1.3.9] and hepatic tryptophan pyrrolase [EC 1.13.1.12; TPO] in rats pre-fed high-protein diets for 5 days and then shifted to zero-protein diets were studied. Liver glucose-6-phosphatase activity decreased 1 day after the dietary shift but then increased and remained significantly higher than the 0 day value for the next 2 days. Changes in liver glycogen were found to be intimately and inversely related to liver glucose-6-phosphatase activity. Changes in kidney glucose-6-phosphatase activity paralleled the pattern of changes observed in liver activity. An initial decrease in TPO activity was followed by increased enzyme activity up to the 3rd day of the dietary shift. Later there was a rapid fall in tryptophan pyrrolase activity. Changes observed in these specific enzyme proteins differed from those observed in total tissue proteins. Alterations in the activities of these enzymes and changes in other parameters are compared with those observed earlier with the reverse type of dietary shift.     

Paradoxical effect of ethanol on liver lipogenesis in the genetically-obese Zucker rat

Sixteen obese (fa/fa) Zucker rats, sixteen lean (Fa/-) Zucker rats and sixteen Wistar rats, all male rats aged 7-8 weeks, were given either a control (C) diet containing no ethanol or an ethanol (E) diet in which 36% of the energy was supplied by ethanol, for a period of 4 weeks. The activities of glucose-6-phosphate dehydrogenase (EC 1.1.1.49), glucose-6-phosphatase (EC 3.1.3.9) and glycerol kinase (EC 2.7.1.30) and the glycogen content in the livers of obese (fa/fa) rats were lower in animals given diet E than in those given diet C. As a result, hepatic lipogenesis and fatty degeneration of the liver were reduced in obese (fa/fa) rats given diet E.     

Nutrition therapy for hepatic glycogen storage diseases

Hepatic glycogen storage diseases (GSD) are a group of rare genetic disorders in which glycogen cannot be metabolized to glucose in the liver because of one of a number of possible enzyme deficiencies along the glycogenolytic pathway. Patients with GSD are usually diagnosed in infancy or early childhood with hypoglycemia, hepatomegaly, poor physical growth, and a deranged biochemical profile. Dietary therapies have been devised to use the available alternative metabolic pathways to compensate for disturbed glycogenolysis in GSD I (glucose-6-phosphatase deficiency), GSD III (debrancher enzyme deficiency), GSD VI (phosphorylase deficiency, which is less common), GSD IX (phosphorylase kinase deficiency), and GSD IV (brancher enzyme deficiency). In GSD I, glucose-6-phosphate cannot be dephosphorylated to free glucose. Managing this condition entails overnight continuous gastric high-carbohydrate feedings; frequent daytime feedings with energy distributed as 65% carbohydrate, 10% to 15% protein, and 25% fat; and supplements of uncooked cornstarch. In GSD III, though glycogenolysis is impeded, gluconeogenesis is enhanced to help maintain endogenous glucose production. In contrast to treatment for GSD I, advocated treatment for GSD III comprises frequent high-protein feedings during the day and a high-protein snack at night; energy is distributed as 45% carbohydrate, 25% protein, and 30% fat. Patients with GSD IV, VI, and IX have benefited from high-protein diets similar to that recommended for patients with GSD III.     

The effect of biotin deficiency and dietary protein content on lipogenesis, gluconeogenesis and related enzyme activities in chick liver

Chicks were given biotin-deficient diets containing either suboptimal (low) or supraoptimal (high) concentrations of protein from 1-d-old until they were used during their fourth week of life. The low-protein diet predisposed chicks to develop fatty liver and kidney syndrome and the high-protein diet to develop classical biotin deficiency signs. Two other groups, as controls, received biotin-supplemented rations. Low dietary protein increased lipogenesis by isolated hepatocytes but had little effect on gluconeogenesis compared to high dietary protein. Low dietary protein decreased activities of hepatic isocitrate dehydrogenase (EC 1.1.1.42), fructose-1,6-bisphosphatase (EC 3.1.3.11) and glucose-6-phosphatase (EC 3.1.3.9; GP) and increased activities of fatty acid synthase (FAS), citrate cleavage enzyme (EC 4.1.3.8; CCE) and malate dehydrogenase (decarboxylating) (EC 1.1.1.39). When biotin deficiency was superimposed, the rate of lipogenesis by isolated hepatocytes (from fed birds) was decreased. Gluconeogenesis from lactate and glycerol was also depressed. Activity of GP was further decreased by biotin deficiency on the low-protein regimen and FAS and CCE were further increased. PK activity was increased by biotin deficiency.     

The role of adrenals in diazinon-induced changes in carbohydrate metabolism in rats

Treatment of rats with diazinon (40 mg/kg, i.p.) resulted in hyperglycaemia and depletion of glycogen from the brain and peripheral tissues two hours after administration. The activities of glycogen phosphorylase and phosphoglucomutase were significantly higher in the brain and liver; that of glucose-6-phosphatase was not altered. The activities of the glycolytic enzymes hexokinase and lactate dehydrogenase were increased only in the brain. The cholinesterase activity in the brain was reduced by treatment with diazinon. The activities of the hepatic gluconeogenic enzymes fructose 1,6-diphosphatase and phosphoenolpyruvate carboxykinase were significantly increased. The lactate level was increased in the brain and blood, whereas that of pyruvate was not changed. The activity of glucose-6-phosphate dehydrogenase was not changed to any major extent. Cholesterol and ascorbic acid contents of adrenals were depleted in diazinon-treated animals. The changes were pronounced after intraperitoneal administration of 40 mg/kg diazinon, they were slight but significant after 20 mg/kg, and absent after 10 mg/kg. Hyperglycaemia and changes in carbohydrate metabolism were abolished by adrenalectomy suggesting possible involvement of adrenals.     

Dietary effects on liver and muscle glycogen repletion in exhaustively exercised rats: energy composition and type of complex carbohydrates

Previous reports have indicated that administration of a glucose-citrate (G-C) drink after a bout of exhaustive exercise results in more effective glycogen repletion in liver and skeletal muscle in rats as compared with administration of glucose alone. The present studies report the effects of the energy pattern and the type of carbohydrates, dextrin or starch from rice, in diet given following the G-C drink after exercise, on further glycogen repletion in the tissues of rats. Rats were adapted to meal-feeding 3 times a day and trained with light swimming for 7 to 10 days. On the final day of experiments, rats received the G-C drink after 2 h of exhaustive swimming and were then fed on diets with different energy patterns or carbohydrate types. Results showed that a high-carbohydrate diet is more effective than a high-fat diet for further glycogen repletion in liver and skeletal muscle. In addition, dextrin was revealed to be superior to starch as a carbohydrate source in tissue glycogen repletion. As compared with the high-fat diet, the high-carbohydrate diet, however, resulted in a lower serum free fatty acid concentration 4 h after ingestion of food possibly by decreasing adipose tissue lipolysis.     

An acute increase in fructose concentration increases hepatic glucose-6-phosphatase mRNA via mechanisms that are independent of glycogen synthase kinase-3 in rats

It appears that low amounts of fructose improve, whereas increased concentrations impair glucose tolerance and hepatic glucose metabolism. In this study, we compared directly the effects of low vs. high portal vein fructose concentrations on hepatic glucose metabolism in rats, using glucose-6-phosphatase gene expression as an endpoint. In the control group (C; n = 7), pancreatic clamps were performed using somatostatin and replacement of insulin such that basal glucose levels were maintained. In the experimental groups (n = 8/group), hyperglycemic, hyperinsulinemic pancreatic clamps were performed in which glucose (G) or glucose + fructose was infused into a jejunal vein. Fructose was infused to achieve either low (F1; <0.3 mmol/L) or high (F2; >1.0 mmol/L) portal vein concentrations. Total sugar load to the liver was equalized among the 3 experimental groups. Compared with C, liver glucose-6-phosphatase catalytic subunit mRNA was reduced by approximately 55% in G and F1, whereas it was increased approximately 180% in F2. F2 did not differentially affect glucose-6-phosphate translocase or phosphoenolpyruvate carboxykinase mRNA levels in liver, nor kidney glucose-6-phosphatase catalytic subunit mRNA. Livers from the F2 group were characterized by an accumulation of pentose phosphate intermediates and reduced phosphorylation of glycogen synthase kinase-3 (active form). However, in separate studies (n = 5/group), the infusion of a glycogen synthase kinase-3 inhibitor did not prevent the effects of F2 on glucose-6-phosphatase gene expression. We hypothesize that elevated fructose concentrations, similar to levels achieved after ingestion of sucrose- or fructose-enriched meals, initiate signals within the liver that elicit selective changes in hepatic gene expression.     

Stoppage of glycogenesis and "over-shoot" of induction of lipogenesis and its related enzyme activities in the liver of fasted-refed rats.

To elucidate the causes of changes of carbohydrate metabolic pathways, the time course of utilization of dietary [U-14C]sucrose and induction of enzyme activities in the livers of rats were investigated. Adult male rats of BHE strain were refed after a fast of 2 days. The nutritionally complete refeeding diet contained 60% sucrose as the only source of carbohydrate. [U-14C]Sucrose was included in the diet on either day 1 or day 2, or both of refeeding. During the first day of refeeding, the radioactivity was incorporated mainly into liver glycogen which rose to over 100 mg/g. During the second day, little 14C appeared in the liver glycogen, which decreased sharply while glucose-6-phosphatase activity increased. The glycogenic pathway thus appeared to be blocked. On the other hand, 14C incorporation in the liver fat was minimal during the first day, but was quite extensive during the second day of refeeding. The enhanced lipogenesis was accompanied by large increases of activities of glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and NADP-malic dehydrogenase. Results clearly indicate that the carbohydrate load in the liver of intact animals was initially metabolized by the glycogenic pathway. When glycogenesis stopped, carbohydrate was metabolized differently. The enhanced incorporation of [U-14C]sucrose into liver lipids indicates an increased formation of acetyl CoA and an accelerated formation and use of NADPH, probably from increasing dehydrogenase activities. Our data suggest that the blockage of synthesis of glycogen with the continuation of carbohydrate load was a primary cause in over-shooting induction of hepatic dehydrogenase activities and lipogenesis.     

Effects of vitamin E deficiency on the activities of lipid-requiring enzymes in rabbit liver and muscle.

The effects of vitamin E deficiency on membrane integrity were studied by examining the temperature dependence of membrane-bound enzyme activities in liver mitochondria and microsome and in muscle sarcoplasmic reticulum. In vitamin E-deficient rabbits, the specific activities at 37 degrees of mitochondrial oligomycin-sensitive ATPase (EC 3.6.1.3), beta-hydroxybutyrate dehydrogenase (EC 1.1.1.30), and microsomal glucose-6-phosphatase (EC 3.1.3.9) were increased, whereas those of microsomal NADH cytochrome C reductase (EC 1.6.99.3) and sarcoplasmic reticulum Ca-ATPase were reduced in comparison to control rabbits. Arrhenius plots of activity against temperature yielded a linear plot over the range 10 to 40 degrees in the case of beta-hydroxybutyrate dehydrogenase, NADH cytochrome C reductase and Ca-ATPase, and multiple discontinuities for glucose-6-phosphatase and oligomycin-sensitive ATPase. In control rabbits, all five enzymes showed a single discontinuity in the Arrhenius plot over the range 16 to 19 degrees. These results reflect changes in the microenvironment of membrane-bound enzymes as a consequence of vitamin E depletion.     

有氧运动调控琥珀酸盐/SUCNR1信号级联改善肥胖相关胰岛素抵抗

目的 探讨有氧跑台运动调控肠道琥珀酸盐/SUCNR1信号改善肥胖相关胰岛素抵抗的作用机制。方法 8周龄雄性C57BL/6和SUCNR1缺失小鼠随机分为对照组、高脂模型组和高脂模型+运动组。对照组和高脂组分别喂食普通膳食和高脂饲料,运动组为连续8周的跑台运动:15米/分,1 h/天,5天/周。结合16s rRNA测序和质谱分析肠道菌群及肠道琥珀酸盐含量;采用血糖检测仪检测血糖和酶偶联反应检测胰岛素、葡萄糖6磷酸（G6P）和糖原（Glycogen）含量;WB检测肠道葡萄糖6磷酸酶（G6Pase）和磷酸烯醇丙酮酸羧激酶（PEPCK）的表达。结果 高脂处理下调肠道琥珀酸盐（99.08±10.99 vs 14.65±4.462）,抑制肠道SUCNR1（下调66%）、G6Pase（下调40%）和PEPCK（下调45%）蛋白表达,促进肝脏G6P表达（1.77倍）和糖原储存（1.68倍）,提示肠道糖异生受到抑制,肝脏糖异生得到提升,诱导胰岛素抵抗;有氧运动干预逆转上述变化,提高胰岛素敏感性。SUCNR1缺失小鼠阻断了有氧运动对肥胖相关胰岛素抵抗的改善作用。结论 有氧运动促进肠道琥珀酸盐,琥珀酸盐/SUCNR1信号通过促进肠道糖异生,降低肝脏糖异生,从而改善肥胖小鼠胰岛素抵抗。     

Fructose Consumption Affects Glucocorticoid Signaling in the Liver of Young Female Rats

The effects of early-life fructose consumption on hepatic signaling pathways and their relation to the development of metabolic disorders in later life are not fully understood. To investigate whether fructose overconsumption at a young age induces alterations in glucocorticoid signaling that might contribute to development of metabolic disturbances, we analysed glucocorticoid receptor hormone-binding parameters and expression of its target genes involved in gluconeogenesis (phosphoenolpyruvate carboxykinase and glucose-6-phosphatase) and lipid metabolism (lipin-1), as well as redox and inflammatory status in the liver of female rats subjected to a fructose-rich diet immediately after weaning. The fructose diet increased hepatic corticosterone concentration, 11β-hydroxysteroid dehydrogenase type 1 level, glucocorticoid receptor protein level and hormone-binding activity, as well as lipin-1 level. The expression of glucose-6-phosphatase was reduced in fructose-fed rats, while phosphoenolpyruvate carboxykinase remained unaltered. The fructose-rich diet increased the level of fructose transporter GLUT2, while the expression of fructolytic enzymes fructokinase and aldolase B remained unaltered. The diet also affected pro-inflammatory pathways, but had no effect on the antioxidant defence system. In conclusion, a fructose-rich diet applied immediately after weaning promoted lipogenesis and enhanced hepatic glucocorticoid signaling, possibly to protect against inflammatory damage, but without an effect on gluconeogenesis and antioxidant enzymes. Yet, prolonged treatment might ultimately lead to more pronounced metabolic disturbances.     

Effect of mercuric chloride on enzyme activities in the digestive system and chemical composition of liver and muscles of the catfish, Heteropneustes fossilis

The effect of a sublethal concentration (0.3 mg/liter) of mercuric chloride on the activities of alkaline phosphatase, acid phosphatase, glucose-6-phosphatase, amylase, maltase, lactase, lipase, trypsin, pepsin, aminotripeptidase, glycylglycine dipeptidase, and glycyl- -leucine dipeptidase in the digestive system of a freshwater catfish, Heteropneustes fossilis, after exposure for 7, 15, and 30 days, and on the percentage composition of total proteins, lipids, glycogen, iron, calcium, inorganic phosphate, water, ash, and vitamins A, D, E, and C in the liver and muscles after 15 and 30 days of exposure was studied. The activities of alkaline phosphatase and glucose-6-phosphatase were significantly decreased while acid phosphatase activity was elevated above the normal level. Significant decreases were also observed in the activities of all the digestive enzymes except for pepsin the activity of which remained unaltered. Maximum inhibition was recorded after 30 days of exposure and the liver was the most affected organ. Total protein and glycogen contents decreased but total lipids increased; calcium, iron, and inorganic phosphate concentrations were below the normal level in fish exposed to mercury. There was significant fall in vitamin A level.     

Antihyperglycemic effect of umbelliferone in streptozotocin-diabetic rats

The present study was designed to investigate the antihyperglycemic effect of Umbelliferone (UMB) in normal and streptozotocin (STZ)-diabetic rats. Diabetes was induced in adult male albino rats of the Wistar strain, weighing 180-200 g, by administration of STZ (40 mg/kg of body weight) intraperitoneally. Diabetic rats showed an increase in levels of blood glucose and glycosylated hemoglobin (HbA(1c)) and activities of gluconeogenic enzymes such as glucose-6-phosphatase and fructose-1,6-bisphosphatase, and a decrease in levels of plasma insulin, hemoglobin (Hb), and liver glycogen and activities of glucokinase and glucose-6-phosphate dehydrogenase. Intraperitoneal administration of UMB (10, 20, and 30 mg/kg of body weight) and glibenclamide (600 micro g/kg of body weight) in 10% dimethyl sulfoxide dissolved in water, for 45 days, produced significantly decreased levels of blood glucose and HbA(1c) and activities of glucose-6-phosphatase and fructose-1,6-bisphosphatase, while elevating levels of plasma insulin, Hb, and liver glycogen and activities of glucokinase and glucose-6-phosphate dehydrogenase to near normal levels in STZ-diabetic rats when compared with normal control rats. Normal rats treated with UMB (30 mg/kg of body weight) also showed a significant effect on glycemic control. Thus, our results show that UMB at 30 mg/kg of body weight possesses a promising antihyperglycemic effect that is comparable with glibenclamide.     

Postprandial glycogen and lipid synthesis in prednisolone-treated rats maintained on high-protein diets with varied carbohydrate levels

OBJECTIVE: The present experiment was designed to study the effect of a high-protein, high-carbohydrate diet versus a high-protein, low-carbohydrate diet on in vivo postprandial glycogen and lipid synthesis of rats treated with prednisolone. METHODS: Thirty-two 6-wk-old male Sprague-Dawley rats were randomly assigned to one of four equal groups: high-protein, high-carbohydrate; high-protein, high-carbohydrate with prednisolone; high-protein, low-carbohydrate; and high-protein, low-carbohydrate with prednisolone. Rats were sham operated or subcutaneously implanted with prednisolone pellets while being maintained on their respective diets (39% of energy from protein) for 6 wk. Food intake and body weight were monitored throughout the experiment. At the end of the feeding period, overnight-fasted rats were fed a test meal and injected with 3H2O to measure in vivo rates of glycogen and lipid synthesis. Final plasma glucose, insulin, and triacylglycerol concentrations and hepatic glycogen content were also measured. RESULTS: Results showed that hepatic glycogen content (milligrams per gram of liver) was similar across all four experimental groups. Total hepatic glycogen synthesis and its percentage synthesis via pyruvate (indirect pathway) were higher in rats maintained on the high-protein, high-carbohydrate diet compared with those on the high-protein, low-carbohydrate diet and this was not substantially affected by prednisolone administration. Hepatic and epididymal fat pad lipid syntheses were not altered by diet or prednisolone treatments. CONCLUSION: Under long-term high-protein conditions, prednisolone administration does not seem to affect hepatic glycogen synthesis, which was increased with the increased carbohydrate content of the diet.     

Studies on the effect of dimecron on the digestive system of a fresh water fish,Channa punctatus

The effect of exposure to a sublethal concentration (0.32 mg/L) of Dimecron® for 20 days on the digestive system of a fresh water teleost fish,Channa punctatus has been studied. The most conspicuous pathological changes in the liver were vacuolation of the cytoplasm of hepatocytes, enlargement of nuclei, rupture of the cell membrane, liver cord disarray, damage of connective tissue, infiltration of phagocytes and necrosis. The mucosa of stomach was ruptured and the gastric glands were degenerated. The mucosal epithelium of intestine and pyloric caeca was also degenerated. The mucus secreting goblet cells showed hyperactivity and the intestinal lumen was filled with mucus. No conspicuous changes were noted in the rectum except for hypersecretion of mucus.Histochemical tests revealed that alkaline phosphatase and glucose-6-phosphatase were inhibited by Dimecron treatment. However, acid phosphatase showed slight increase in activity. Biochemical tests for enzyme activity confirmed the histochemical findings. Alkaline phosphatase activity was significantly inhibited in liver and intestine. There was a slight elevation in the activity of acid phosphatase in the liver and pyloric caeca of exposed fish, but this was not statistically significant. The glucose-6-phosphatase activity was significantly inhibited in the liver, intestine and pyloric caeca.     

The effect of an unsaturated-fat diet on cataract formation in streptozotocin-induced diabetic rats.

1. Cataract formation in streptozotocin-induced diabetes in rats was reduced by approximately 85% when a diet rich in maize oil (300 g/kg diet) (fat diet) was given, thus confirming results of earlier studies. However, the concentration of sorbitol in the lens of diabetic animals remained high, the values for diabetic rats given the standard diet and the fat died being 65 and 40 mumol/g protein respectively. 2. With the standard diet, the fatty acid profile of the triglycerides of the epididymal fat pads was characterized by a greater relative proportion of saturated fatty acids for the diabetic animals compared to that for the normal animals. The fat diet moderated the tendency towards saturation in the diabetic animals. 3. The fat diet had other effects on the diabetic animals; these included a reduced mortality rate, increased body-weight, a decrease in the daily water intake, and in the daily urinary excretion of glucose and urea. 4. In the diabetic animals the fat diet had no effect on the specific activities in the liver of hexokinase (EC 2.7.1.1), glucokinase (EC 2.7.1.2), phosphofructokinase (EC 2.7.1.11) and pyruvate kinase (EC 2.7.1.40). However, the specific activity of glucose-6-phosphatase (EC 3.1.3.9) was reduced, while that of malate dehydrogenase (decarboxylating) (NADP) (EC 1.1.1.40) was increased. The NAD+:NADH ratio, as calculated from liver pyruvate and lactate concentrations, tended to increase. 5. The results suggested that the fat diet moderated the long-term metabolic effects of diabetes.     

Examination of dynamic changes of certain biochemical parameters in blood of rats poisoned with sodium nitrite]

In Wistar rats poisoned by daily addition of sodium nitrite to drinking water (1 g/dm3), determination was made of the dynamics of changes in: blood methemoglobin and 2,3-diphosphoglyceric acid levels, contents of protein and non-protein thiol groups in erythrocytes, blood glucose-6-phosphate dehydrogenase and peroxide dismutase activities, as well as plasma vitamin E and hydroxyproline levels, Determinations were performed after 15, 30, 45, 60, 75 and 90 days of poisoning. There occurred a linear relationship between the drop in glucose-6-phosphatase dehydrogenase activity and in vitamin E level, on one hand, and the duration of poisoning with sodium nitrite. Moreover, a significant rise of 2,3-diphosphoglyceric acid level in erythrocytes and a decrease in the non-protein thiol groups took place. Rhe results indicated that the determinations--in blood--of: methemoglobin, glucose-6-phosphate dehydrogenase activity in erythrocytes, and vitamin E in plasma or serum, could be included among the diagnostic tests performed (at the laboratories attached to industrial plants or making part of the industrial health service) for evaluation of the health hazard in the nitro-compound industry or in other nitrite contaminated working places.     

Absence of effects of dietary wheat bran on the activities of some key enzymes of carbohydrate and lipid metabolism in mouse liver and adipose tissue

1. The effects of a 100 g/kg dietary substitution of wheat bran on the body-weight gain, food consumption and faecal dry weight of mice given a high-sucrose diet and on the activities of some key enzymes of carbohydrate and lipid metabolism in liver and adipose tissue were studied. 2. Wheat bran had no effect on body-weight gain, food consumption or faecal dry weight. 3. Wheat bran had no effect on the activities of hepatic glucose-6-phosphate dehydrogenase (EC 1.1.1.49), 6-phosphogluconate dehydrogenase (EC 1.1.1.44), malate dehydrogenase (oxaloacetate-decarboxylating) (NADP+) (EC 1.1.1.40), ATP-citrate (pro-3S)-lyase (EC 4.1.3.8), pyruvate kinase (EC 2.7.1.40) and fructose-1,6-bisphosphatase (EC 3.1.3.11). The activity of hepatic 6-phosphofructokinase (EC 2.7.1.11) increased but only when expressed on a body-weight basis. 4. Wheat bran had no effect on the activities of adipose tissue glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, malate dehydrogenase (oxaloacetate-decarboxylating) (NADP+), ATP-citrate (pro-3S)-lyase, hexokinase (EC 2.7.1.1), 6-phosphofructokinase and pyruvate kinase. 5. These results suggest that unlike guar gum and bagasse, wheat bran does not change the flux through some pathways of lipogenesis in liver and adipose tissue when mice are given high-sucrose diets.     

Human adipose tissue glycogen levels and responses to carbohydrate feeding

Glycogen has long been known to be present in adipose tissue, but its role is not clear. It has not been measured in human adipose tissue. We have investigated methods for its measurement using rat adipose tissue, and measured levels in humans. Glycogen in rat adipose tissue was found to be labile, necessitating rapid sample preservation. Levels in random biopsies of human adipose tissue were variable, but consistent with values for other species (0.06-0.78 mg/g wet weight; n = 5). After overnight fast, consistent low levels were found (0.04-0.08 mg/g wet weight; n = 6); these increased after eating a high-carbohydrate diet (800 g/d for 2.5 d), to 0.10-1.95 mg/g wet weight (P less than 0.05). Human adipose tissue glycogen appears to play a minor role in whole-body glucose homeostasis, but may have an important local role in the regulation of lipogenesis.     

Carbohydrate Free Diet In Rats

Young rats fed for one week a diet free of carbohydrate and limited in carbohydrate precursors developed increased gluconeogenesis and decreased glucose utilization. Activities of glucose-6-phosphatase, fructose-1,6-diphosphatase, and glutamic-pyruvic transaminase in the liver were enhanced, while glucokinase activity and glucose tolerance were decreased.