Dietary carbohydrate level and glucose metabolism in turkey poults.

1. Feeding British United turkeys (BUT) and Nicholas turkeys (NT) diets with varying carbohydrate levels for 24 hr post-hatch resulted in lower hepatic glucose-6-phosphatase activity and higher plasma glucose levels as dietary carbohydrate level was increased. 2. There were no differences between the strains in liver weight or glucose-6-phosphatase activity, but BUT exhibited higher plasma glucose values than did NT at the two highest levels of carbohydrate. Plasma glucose did not differ between strains at the lowest level of carbohydrate or in fasted poults. 3. Blood glucose values were consistently higher in both strains when sampled 1 hr after initial sampling of fasted poults. 4. Both strains were able to maintain the 1 hr blood glucose levels through 24 hr when kept at approximately 37 degrees C. 5. When held at approximately 21 C for the first hour and at approximately 37 degrees C through 24 hr fasted NT were able to maintain the initial blood glucose rise while BUT were not.     

Effect of starvation on nutrition and insulin secretion in pregnant rats and their fetuses

Pregnancy is thought to create a metabolic condition of accelerated starvation. To clarify this idea, the effect of fasting on pregnant rats (day 21 of gestation) and their fetuses was examined. Although pregnancy significantly increased plasma insulin, plasma ketone body concentrations in fed pregnant rats were higher than those of age-matched fed virgin rats. After 48 hr fasting (i.e., fasting during days 19-21 of gestation), plasma insulin was markedly decreased in virgin rats compared with term pregnant rats, while ketone bodies were significantly higher in pregnant rats than in virgin rats. Body weight was lower in fetuses from fasted mothers than those from fed mothers. Starvation also markedly diminished the insulin response to glucose in isolated, perfused pancreases in both virgin and pregnant rats. The amount of insulin released during glucose stimulation was greater in pregnancy, and the inhibitory effect of 48 hr fasting on insulin release was greater in virgin rats than in pregnant rats. It is possible, therefore, that in term pregnant rats a decrease in insulin release caused by fasting may cause more profound catabolism than in nongravid rats.     

Effects of hypo and hyperthyroidism on the response to glucose loading of blood glucose, ketones and insulin and liver glycogen as studied in the fasted rat

After receiving an i.p. glucose load, 24 h fasted thyroidectomized rats showed a progressive increase in blood glucose and a slow decrease in blood ketone bodies. Both liver glycogen and plasma insulin levels showed no differences within 60 min of the glucose administration. It is suggested that the glucose intolerance in these animals is partly due to an insulin deficiency. Thyroidectomized rats treated daily with 25 microgram of L-thyroxine/100 g body weight for 40 days responded to the glucose test with a supranormal and more persistent elevation of blood glucose but with a faster and a greater fall in blood ketone bodies, as compared to controls. Sixty min after the glucose loading, liver glucogen levels were lower and plasma insulin were slightly higher than controls. It is suggested that a diminished extraction of glucose during transhepatic passage can be responsible for the impaired glucose tolerance observed in the hyperthyroid animals.     

Differential effects of fatty acids and exercise on body weight regulation and metabolism in female Wistar rats

High-fat diets made with different fats may have distinct effects on body weight regulation and metabolism. In the present study, the metabolic effects of high-fat (HF) diets made with fish oil, palm oil, and soybean oil were compared with a low-fat diet in female Wistar rats that were either exercised (EX, swimming) or that remained sedentary as controls. Each adult rat was exposed to the same diet that their dams consumed during pregnancy and lactation. When they were 9 weeks old, rats began an EX regimen that lasted for 6 weeks. Twenty-four hours after the last EX bout, rats were sacrificed in a fasted state. It was observed that HF feeding of soybean oil induced more body weight and fat gain, as well as insulin resistance, as indicated by insulin/glucose ratios, than other oils. Female rats fed a HF diet made with fish oil had body weight and insulin sensitivity not different from that observed in low fat fed control rats. For rats fed HF diets made with soybean oil or palm oil, EX also exerted beneficial effects by reducing body fat %, blood insulin, triglyceride and leptin levels, as well as improving insulin sensitivity.     

Glucose supplement reverses the fasting-induced suppression of cellular immunity in Mongolian gerbils (Meriones unguiculatus)

Glucose plays an important role in immunity. Three day fasting will decrease cellular immunity and blood glucose levels in Mongolian gerbils (Meriones unguiculatus). In the present study, we tested the hypothesis that glucose supplement can reverse the fasting-induced suppression in cellular immunity in gerbils. Twenty-eight male gerbils were selected and randomly divided into fed and fasting groups. Half of the gerbils in each group were then provided with either 10% glucose water or pure water. After 66 h, each gerbil was injected with phytohaemagglutinin (PHA) solution to challenge cellular immunity. Results showed that glucose supplement restored blood glucose levels in fasted gerbils to those of the fed controls. It also recovered cellular immunity, body fat mass and serum leptin levels in fasted gerbils to the values of the fed controls. Blood glucose levels were positively correlated with body fat mass, leptin levels and cellular immune responses. Thymus and spleen masses, and white blood cells in fasted gerbils were not affected by glucose supplement. In general, our data demonstrate that glucose supplement could reverse fasting-induced suppression of cellular immunity in Mongolian gerbils.     

In vitro glucose reversal of the inhibitory effect of fasting on epinephrine-induced lipolysis

Cyclic AMP, protein kinase activity and glycerol were measured in adipose tissue from fasted rats incubated with epinephrine with or without glucose. A drastic loss in the sensitivity of the adipose tissue to respond to the lipolytic action of the hormone was observed during fasting, when incubated without glucose. The addition of glucose reverses this process, and a greater lipolytic capacity was observed in the tissue of fasted rats than in fed rats. The three parameters measured were well correlated when there was epinephrine in the medium. Lipolysis is observed with glucose alone, but there was no variation in the cAMP levels nor in the protein kinase activity. These results are discussed in relation to the regulator effect of FFA, which is mobilized during starvation, on lipolysis.     

Effect of starvation of gastric somatostatin release

The present study is an investigation of the effects of 16 and 48 hours starvation on gastric somatostatin release using the isolated perfused rat stomach. Before sacrifice the body weights and blood glucose levels of fasted rats were significantly lower than fed rats. In the presence of 4.4 mM glucose, basal somatostatin concentrations in the stomach perfusate of fasted rats were also significantly lower. Gastric somatostatin release was stimulated in all three groups similarly by 5 × 10^?8 M glucagon when the decrease in basal levels is considered. These results suggest that gastric somatostatin as well as pancreatic somatostatin contributes to nutrient homeostasis and that nutrient homeostasis influences somatostatin levels in turn.     

Blood glucose and serum insulin levels in lean and genetically obese mice.

Fed and 24 hour fasted lean and genetically obese mice (ob/ob) were given a fixed glucose load per gm body weight by intraperitoneal and intragastric administration. Intraperitoneal glucose injection into the obese mice produced a prolonged elevated blood glucose level with a concomitant significant decrease of circulating insulin. Possible interpretations of this observation are discussed. In those obese animals in which glucose was administered intragastrically the fed obese mice had a blood glucose concentration of 450-500 mg% for a period of one hour but there was no increase in circulating insulin, however, in the fasted obese mice in which the glucose concentration was about 350 mg% for one hour, there was a significant increase in the circulating insulin levels. The fed and fasted lean mice showed normal glucose tolerance curves and the expected increase in circulating insulin following either intraperitoneal orintragastric glucose loads. It is concluded that hyperglycaemia in the ob/ob mice is unlikely to be the principal cause of hyperinsulinaemia.     

Glucose turnover and defense of blood glucose levels in Arctic fox (Alopex lagopus)

1. Glucose utilization was assessed in fed and fasted arctic fox, maintained on a diet similar in composition to food available in the wild. 2. Fasted (24 hr) glucose concentration was not significantly different from the fed level (134 mg/dl). 3. Fasting was associated with a significant reduction in glucose space, pool size, total entry rate, and irreversible loss which suggests a decline in gluconeogenesis. 4. Glucose recycling was not significantly different between the fed and fasted states. 5. We suggest that, in the arctic fox, the mechanism for defending blood glucose levels during fasting is based on restricting blood glucose to tissues with a high glucose dependency.     

Insulinotropic and gastrin-releasing action of gastrin-releasing peptide (GRP)

The effect of intravenous administration of gastrin-releasing peptide ( GRP ) on serum gastrin and insulin levels was studied in ad libitum fed and 24-h fasted rats. Administration of GRP (55 micrograms/kg body weight) caused a significant (P less than 0.05) elevation in serum gastrin levels at 10, 30, 60, and 120 min in the rats fed ad libitum, whereas in the fasted rats, gastrin levels rose significantly only at 10 min. GRP did not cause insulin release in fasted rats, but in the fed rats, it led to a significant elevation in serum insulin levels at 10 and 30 min, in comparison to controls. GRP appears to have an insulinotropic action in addition to a gastrin-releasing effect.     

Circadian rhythm of ketone bodies in the blood of fasting rats

SPF male Wistar rats were kept under standard conditions with a light: dark schedule of 12:12 h. The total ketone body concentration was determined in the blood, and the non-esterified fatty acid level in the serum, of fed rats and of animals which had fasted 24 and 48 h. The amount of ketone bodies in fed rats rose in the second half of the light period and fell with the onset of the dark period. After a 24 h fast, the amount of ketone bodies in the blood rose, but the basic characteristics of the curve and the rhythm remained the same as in fed animals. After a 48 h fast, the mean ketone body concentration was decoupled, a significant phase shift occurred and the rhythm was lost. No relationship between the oscillations of the total ketone body concentration in the blood and the oscillations of the serum non-esterified fatty acid level was found.     

Stimulation of anaerobic metabolism in rats at high altitude hypoxia--adrenergic effects dependent on dietary states

1. Plasma lactate and pyruvate were increased more markedly in fed rats than in fasted rats exposed to an 8000 m altitude. 2. The increase in plasma lactate and pyruvate was enhanced and inhibited by the alpha 1-adrenergic antagonist prazosin and the beta-blocker propranolol, respectively, in fasted rats exposed to an 8000 m altitude. Blood glucose was not changed by adrenergic blockades under the same conditions. 3. Prazosin and propranolol showed no effect on glycolytic metabolites in plasma in fed rats submitted to an 8000 m altitude. Blood glucose of fed rats was increased by alpha 1-blockade during severe hypoxia. 4. In fasted rats whose energy metabolism depends on oxidation mainly, alpha 1- and beta-adrenergic receptors can participate in the stimulation of respiration and the glycogen degradation, respectively, during an exposure to severe hypoxia. In fed rats energy metabolism depends on glycolysis, which utilizes blood glucose as the substrate preferentially during hypoxia.     

Leptin responses to glucose infusions in obesity-prone rats

The secretion of leptin is dually regulated. In fasting animals, plasma leptin concentrations reflect body fat stores, whereas the incremental leptin response to fasting or refeeding most likely reflects insulin-mediated energy flux and metabolism within adipocytes. Impaired secretion of leptin in either pathway could result in obesity. We therefore measured plasma leptin concentrations in fasted animals and plasma leptin concentrations after an intravenous glucose infusion in a rat model of obesity. Young Sprague-Dawley (S-D) and Fischer 344 (F344) rats had similar percent body fat and fasting glucose and fasting leptin concentrations. However, F344 animals had higher insulin concentrations and leptin responses to intravenous glucose than did the S-D animals. The animals were then fed a control or high-fat diet for 6 wk. High-fat fed animals gained more weight and body fat than did the control fed animals. Control and high-fat fed F344 animals gained approximately 40% (P < 0.0001) more weight and >100% (P < 0.01) more body fat than did the S-D animals. Fasting leptin concentrations and leptin concentrations after intravenous glucose infusions and feeding were more than double (P < 0.05) in F344 animals compared with S-D animals. Whether an animal is fed a control or high-fat diet had little effect on the leptin response to intravenous glucose. In conclusion, young, lean F344 animals, before the onset of obesity, demonstrated a greater acute leptin response to intravenous glucose than similarly lean S-D animals. After a 6-wk diet, F344 animals had a greater percent increase in body weight and insulin resistance and exhibited higher fasting leptin concentrations and a greater absolute leptin response to intravenous glucose compared with the S-D animals. The chronic diet (control or high fat) had little impact on the acute leptin response to intravenous glucose. F344 animals exhibit leptin resistance in young, lean animals and after aging and fat accumulation.     

瘦素基因敲除肥胖大鼠的血糖及病理长期观察

目的：对Leptin基因敲除SD大鼠血糖变化及病理表型进行长期分析,为使用该大鼠作为糖尿病和脂代谢模型积累数据。方法 western blot检测Leptin＋/＋大鼠和Leptin-/-大鼠肝脏中Leptin的表达。利用称量方法测定Leptin基因敲除的SD大鼠（Leptin-/-）1,3,6,8月龄的体重变化,利用稳豪血糖仪采尾血测定1,3,6,8月龄Leptin-/-大鼠空腹血糖值。 HE染色和免疫组织化学观察Leptin-/-大鼠胰腺及肝脏的病理学变化。结果 Leptin-/-大鼠肝脏中表达变短的功能异常的Leptin蛋白。 Leptin-/-大鼠从1月龄开始出现显著的体重增加,8月龄时雌性体重为884 g,雄性体重可以达到1200 g,是野生SD大鼠的2倍。自1月龄起, Leptin-/-雌鼠的空腹血糖值显著高于野生大鼠,在1月龄到6月龄之间差别明显（40％～26％）,到8月龄和野生大鼠恢复到近正常水平。8月龄Leptin-/-大鼠肝脏肝小叶中出现大量脂肪空泡,胰腺内较多脂肪细胞浸润、胰岛数量明显增多,体积增大,胰岛素阳性β细胞增多。结论 Leptin-/-大鼠表型表现为肥胖,脂肪肝,胰岛增生和早期高血糖。     

GK糖尿病大鼠生物学特性观察

目的了解2型糖尿病模型GK大鼠生长曲线、主要脏器重量、糖代谢等生物学特性,评价GK大鼠葡萄糖刺激的胰岛素分泌能力。方法采用51只雄性GK大鼠及15只年龄性别匹配的Wistar大鼠作为研究对象。测定13周龄GK、Wistar大鼠空腹血糖、23周龄GK大鼠空腹及随机血糖。随访GK及Wistar大鼠生长曲线,34～46周龄期间血糖、糖化血红蛋白。46周龄时行腹腔葡萄糖耐量实验（IPGTT）,计算相关参数评价β细胞葡萄糖刺激的胰岛素分泌能力;之后处死大鼠,脏器称重。比较GK及Wistar大鼠间上述各指标差异。结果13周龄GK大鼠空腹血糖4．74±0．41mmol／L,对照Wistar大鼠1．85±0．44mmol／L（P〈0．001）。23周龄GK大鼠空腹血糖7．88±1．96mmol／L,随机血糖9．91±3．52～13．46±4．13mmol／L。7～20及34～45周龄期间GK大鼠体重高于对照Wistar大鼠（P〈0．05）,46周龄时无显著性差异。34～45周龄期间GK大鼠空腹血糖、进食后血糖、HbAlc均高于对照Wistar大鼠（P〈0．05）。IPGTT曲线下面积分析示GK大鼠胰岛素曲线下面积（AUCi）、葡萄糖曲线下面积（AUCg）高于对照Wistar大鼠,胰岛素与葡萄糖曲线下面积比值（AUCi／AUCg）低于对照Wistar大鼠,差异均有显著性（P〈0．05）。GK大鼠肾脏重量高于对照Wistar大鼠（P〈0．05）,余主要脏器重量差异无显著性。结论GK大鼠空腹血糖、进食后血糖、HbAlc水平升高,葡萄糖刺激的胰岛素分泌能力（GSIS）减退,葡萄糖刺激后胰岛素分泌早期相消失,晚期相代偿性增加,具有2型糖尿病特点;体重、血糖等生物学特性稳定。     

Circadian rhythm of blood glucose and tissue glycogen in fed and fasted rats

Blood glucose and tissue glucogen circadian rhythms were determined in male Wistar rats adapted 3 weeks to an artificial lighting regimen of 12 hours' light and 12 hours' darkness. Over a period of 24 hours we examined at 3-hour intervals the blood glucose concentration and the glycogen content of the liver, heart, skeletal muscle (quadriceps femoris) and white (epididymal) and brown (interscapular) adipose tissue of fed rats and rats fasted for 24 hours. The experiments were carried out in the autumn and the results were evaluated statistically by an analysis of variance and the cosinor test. The blood glucose level and the glycogen concentration in all the given tissues, in both fed and starved rats, displayed rhythmic oscillations with a 24- or 12-hour period in the course of the day, with the exception of glycogen in the white adipose tissue of fed rats, in which cosinor analysis failed to demonstrate any rhythm. One day's fasting did not affect the character of circadian rhythm.     

Effects of oral administration of benzylamine on glucose tolerance and lipid metabolism in rats

Repeated administration of benzylamine plus vanadate have been reported to exhibit anti-hyperglycemic effects in different models of diabetic rats. Likewise oral treatment withMoringa oleifera extracts which contain the alkaloïd moringine, identical to benzylamine, has also been shown to prevent hyperglycemia in alloxan-induced diabetic rats. With these observations we tested whether prolonged oral administration of benzylamine could interact with glucose and/or lipid metabolism. Seven week old male Wistar rats were treated for seven weeks with benzylamine 2.9 g/l in drinking water and were submitted to glucose tolerance tests. A slight decrease in water consumption was observed in benzylamine-treated animals while there was no change in body and adipose tissue weights at the end of treatment. Blood glucose and plasma insulin, triacylglycerol or cholesterol levels were not modified. However, benzylamine treatment resulted in a decrease in plasma free fatty acids in both fed and fasted conditions. Benzylamine treatment improved glucose tolerance as shown by the reduction of hyperglycemic response to intra-peritoneal glucose load. Oral benzylamine treatment did not alter the response of adipocytes to insulin nor to insulin-like actions of benzylamine plus vanadate, viain vitro activation of glucose transport or inhibition of lipolysis. This work demonstrates for the first time that oral administration of benzylamine alone influences glucose and lipid metabolism. However, these results obtained in normoglycemic rats require to be confirmed in diabetic models.     

Influence of fasting on glycogen depletion in rats during exercise

We recently observed that a 24-h fasted group of rats could run longer than an ad libitum fed control group before becoming exhausted. Because of the demonstrated importance of glycogen levels and free fatty acid availability during endurance exercise, we have investigated several parameters of carbohydrate and lipid metabolism in exercised and nonexercised rats that were either fed ad libitum or fasted for 24 h. A 24-h fast depleted liver glycogen, lowered plasma glucose concentration, decreased muscle glycogen levels, and increased free fatty acid and beta-hydroxybutyrate concentrations in plasma. During exercise the fasted group had lower plasma glucose concentration, higher plasma concentration of free fatty acids and beta-hydroxybutyrate, and a lower muscle glycogen depletion rate than did the ad libitum fed group. Since fasted rats were able to continue running even when plasma glucose had dropped to levels lower than those of fed-exhausted rats, it seems unlikely that blood glucose level, per se, is a factor in causing exhaustion. These results suggest that fasting increases fatty acid utilization during exercise and the resulting "glycogen sparing" effect may result in increased endurance.     

Reciprocal changes of plasma glucose and ketone bodies in fasted and acutely diabetic rats after CNS stimulation

To assess the effect of chemical stimulation of the central nervous system (CNS) on ketogenesis, we injected neostigmine (5 x 10(-8)mol) into the third cerebral ventricle in normal rats fasted for 48 h and fed rats with diabetes induced by streptozotocin (STZ, 80 mg/kg). The hepatic venous plasma levels of ketone bodies (3-hydroxybutyrate and acetoacetate), free fatty acids (FFA), and glucose were measured for 120 min after the injection of neostigmine under pentobarbital anesthesia. In the normal rats, plasma glucose levels were significantly increased but neither ketone bodies nor FFA were affected by CNS stimulation with neostigmine. In contrast the plasma levels of ketone bodies and FFA were significantly increased in STZ-diabetic rats, while glucose levels remained unchanged. The intravenous infusion of somatostatin (1.0 microgram/kg/min) suppressed the increase in plasma ketone bodies following CNS stimulation in STZ-diabetic rats. These findings suggest that CNS stimulation with neostigmine may accelerate ketogenesis by promoting the lipolysis, which may be induced by glucagon, in fed diabetic rats but not in normal fasted rats.     

Thyroxine effects on parameters of glucose turnover in BHE rats fed menhaden oil

The effect of hyperthyroidism on glucose turnover in BHE rats fed menhaden oil was studied. Thyroxine-treated rats had a greater glucose mass, a greater absolute glucose synthesis rate, less hepatic and muscle glycogen levels, and greater hepatic and peripheral fat cell lipogenic rates than nontreated rats. No differences in body weight gain were observed, nor were there differences in blood glucose levels, glucose space, or fractional reversible or irreversible glucose use. These observations suggest that thyroxine and menhaden oil were additive in their effects on glucose metabolism in BHE rats, which are genetically programmed to develop non-insulin-dependent diabetes mellitus.