Exceptionally low blood glucose response to dried beans: comparison with other carbohydrate foods.

Normal volunteers took 50-g carbohydrate portions of eight varieties of dried legumes and 24 common foods drawn from grains, cereals and pasta, breakfast cereals, biscuits, and tuberous vegetables. Both the mean peak rise in blood glucose concentrations and mean area under the glucose curve of the subjects who ate beans were at least 45% lower than those of subjects who ate the other foods. These results suggest a potentially valuable role for dried leguminous seeds in carbohydrate exchanges for individuals with impaired carbohydrate tolerance.     

Studies on oral glucose intolerance in fish

The oral glucose tolerance test, a diagnostic procedure used in the detection of human diabetes, was used to study carbohydrate metabolism in rainbow trout, Salmo gairdneri (Richardson). Fish exhibited pronounced and persistent hyperglycaemia on oral glucose administration. Hyperglycaemia was accompanied by decrease in blood amino acids, serum free fatty acids and cholesterol and marked increase in hepatic storage of glycogen. The incidence of oral glucose intolerance results, at least in part from insufficient circulating insulin. Exogenous insulin exerts a hypoglycaemic action and effectively abolishes the hyperglycaemia resulting from glucose administration. Tolbutamidc, the sulphonylurea hypoglycaemic drug, is without effect. Possibly as an indirect result of hyperadreno-corticism, oral glucose tolerance is markedly improved in the pre-spawning female. Long-term feeding of high carbohydrate diet to goldfish Carassius auratus (L.) resulted in gross hepatomegaly due to excessive hepatic glycogen accumulation and, possibly, fatty change of the liver. Protein metabolism was impaired as evidenced by protein depletion. Such degenerative changes in liver metabolism are probably a direct result of oral glucose intolerance and reflect a metabolism adapted to diets normally low in available carbohydrate.     

Partial restoration of dietary fat induced metabolic adaptations to training by 7 days of carbohydrate diet.

We tested the hypothesis that a shift to carbohydrate diet after prolonged adaptation to fat diet would lead to decreased glucose uptake and impaired muscle glycogen breakdown during exercise compared with ingestion of a carbohydrate diet all along. We studied 13 untrained men; 7 consumed a high-fat (Fat-CHO; 62% fat, 21% carbohydrate) and 6 a high-carbohydrate diet (CHO; 20% fat, 65% carbohydrate) for 7 wk, and thereafter both groups consumed the carbohydrate diet for an eighth week. Training was performed throughout. After 8 wk, during 60 min of exercise (71 +/- 1% pretraining maximal oxygen uptake) average leg glucose uptake (1.00 +/- 0.07 vs. 1.55 +/- 0.21 mmol/min) was lower (P < 0.05) in Fat-CHO than in CHO. The rate of muscle glycogen breakdown was similar (4.4 +/- 0.5 vs. 4.2 +/- 0.7 mmol. min(-1). kg dry wt(-1)) despite a significantly higher preexercise glycogen concentration (872 +/- 59 vs. 688 +/- 43 mmol/kg dry wt) in Fat-CHO than in CHO. In conclusion, shift to carbohydrate diet after prolonged adaptation to fat diet and training causes increased resting muscle glycogen levels but impaired leg glucose uptake and similar muscle glycogen breakdown, despite higher resting levels, compared with when the carbohydrate diet is consumed throughout training.     

Effects of maternal diabetes on the development of carbohydrate metabolizing enzymes in fetal rat liver

Effects of streptozotocin-induced maternal diabetes on fetal hepatic carbohydrate-metabolizing enzyme development and hormonal status has been explored in the rat. Hepatic glycogen synthase a activity of the normal fetus rose to a maximum at 20 days of gestation, then fell prior to parturition. In fetuses of diabetic mothers, this prepartum decline was curtailed, resulting in enhanced synthase a activity and increased glycogen content in fetal livers at term. Elevation in hepatic synthase a in fetuses of diabetic mothers was due, not to altered interconversion between existing synthase a and b, but to equivalent increases in both forms of the enzyme. Both hepatic and free plasma corticosterone levels were elevated in fetuses of diabetic mothers and may be responsible for the enhanced development of total glycogen synthase observed in these fetuses. In normal fetuses hepatic phosphofructokinase and pyruvate kinase activities also rose to maxima at 20 days, then declined prior to term. In fetuses of diabetic mothers pyruvate kinase activity attained higher than normal maximal levels and phosphofructokinase activity fell more gradually, thus resulting in elevations in both enzyme activities at term. Augmentations in these glycolytic enzymes are compatible with hyperinsulinemia observed in fetuses of diabetic mothers. The following conclusions may be drawn from these findings. During late fetal life developmental patterns of rate-limiting hepatic glycogen-synthesizing and glycolytic enzymes are adapted to glucose utilization. In the normal fetus these patterns reverse at term, thereby promoting glucose mobilization, which prepares the fetus for abrupt deprivation of maternal glucose at birth. Maternal diabetes results in retardation of these reversal processes, presumably due to elevations in fetal glucocorticoid and insulin levels. Glycogenolytic and glucogenic capacities are thereby impaired in these fetuses.     

Longitudinal Adaptations to Very Low–carbohydrate Weight‐reduction Diet in Obese Rats: Body Composition and Glucose Tolerance

Longitudinal effects of a very low–carbohydrate (VLC) and a calorie‐matched high‐carbohydrate (HC) weight reduction diet were compared in dietary obese Sprague–Dawley rats exhibiting impaired glucose tolerance and insulin resistance. Obese rats were divided into weight‐matched groups: (i) VLC rats consumed an energy‐restricted 5% carbohydrate, 60% fat diet for 8 weeks, (ii) HC rats consumed an isocaloric 60% carbohydrate, 15% fat diet, and (iii) HF rats consumed a high‐fat diet ad libitum. HC and VLC rats showed similar reductions in body fat and hepatic lipid at the midpoint of the weight‐reduction program, indicating effects due to energy deficit. At the end point, however, HC rats showed greater reductions in total and percent body fat, hepatic lipid and intramuscular lipid than did VLC rats, suggesting that diet composition induced changes in the relative efficiencies of the HC and VLC diets over time. HC rats showed marked improvement in glucose tolerance at the midpoint and end point, whereas VLC rats showed no improvement. Impaired glucose tolerance in VLC rats at the end point was due to insulin resistance and an attenuated insulin secretory response. Glucose tolerance in energy‐restricted rats correlated negatively with hepatic and intramuscular lipid levels, but not visceral or total fat mass. These findings demonstrate that adaptations to diet composition eventually enabled HC rats to lose more body fat than VLC rats even though energy intakes were equal, and suggest that the elevated levels of hepatic and intramuscular lipid associated with VLC diets might predispose to insulin resistance and impaired glucose tolerance despite weight loss.     

Perturbations in the biochemical composition of fetal fluids are apparent in surviving bovine somatic cell nuclear transfer pregnancies in the first half of gestation

Amniotic and allantoic fluid volumes and composition change dynamically throughout gestation. Cattle that are pregnant with somatic cell nuclear transfer (NT) fetuses show a high incidence of abnormal fluid accumulation (particularly hydrallantois) and fetal mortality from approximately midgestation. To investigate fetal fluid homeostasis in these pregnancies, Na, K, Cl, urea, creatinine, Ca, Mg, total PO(4), glucose, fructose, lactate, total protein, and osmolalities were measured in amniotic and allantoic fluids collected at Days 50, 100, and 150 of gestation from NT pregnancies and those generated by the transfer of in vitro-produced embryos or by artificial insemination. Deviations in fetal fluid composition between NT and control pregnancies were apparent after placental and fetal organ development, even when no gross morphological abnormalities were observed. Individual NT fetuses were affected to varying degrees. Elevated allantoic Na was associated with lower K and increased allantoic fluid volume or edema of the fetal membranes. Total PO(4) levels in NT allantoic and amniotic fluid were elevated at Days 100 and 150. This was not accompanied by hypophosphatemia at Day 150, suggesting that PO(4) acquisition by NT fetuses was adequate but that its readsorption by the kidneys may be impaired. Excessive NT placental weight was associated with low allantoic glucose and fructose as well as high lactate levels. However, the fructogenic ability of the NT placenta appeared to be normal. The osmolality of the fetal fluids was maintained within a narrow range, suggesting that the regulation of fluid composition, but not osmolality, was impaired in NT pregnancies.     

Carbohydrate metabolism is not impaired after 3 years of growth hormone therapy in children with Prader-Willi syndrome

BACKGROUND/AIM: In children with Prader-Labhart-Willi syndrome (PWS), the insulin secretion is reduced, despite obesity, being ascribed to the growth hormone (GH) deficiency of hypothalamic origin. Besides, an increased prevalence of diabetes mellitus was described in this syndrome. Hence, we addressed the questions of how body composition and insulin secretion are interrelated and what impact GH therapy has on the carbohydrate metabolism in PWS. METHODS: We measured weight, lean and fat mass (by dual-energy X-ray absorptiometry), triglycerides, HbA(1c), and fasting insulin and glucose levels in 17 children (age range 1.5-14.6 years) with PWS to examine whether the carbohydrate metabolism is altered during 36 months of therapy with 8 mg GH/m(2) body surface/week. In a subgroup of 8 children, the insulin secretion was longitudinally assayed during oral glucose tolerance at 0 and 12 months of therapy. RESULTS: Before therapy, the insulin secretion was lower and markedly delayed as compared with reference data and did not rise during therapy. The glucose tolerance was impaired in 2 of 12 children examined by oral glucose tolerance test before therapy and normalized during therapy. Fasting insulin and insulin resistance being normal at the beginning, significantly increased at 12 months and returned to initial levels at 36 months of GH therapy. Fasting glucose as well as HbA(1c) and triglyceride levels were always normal. The fat mass before GH therapy was increased (39.5%) and dropped into the upper normal range (28.3%) during 3 years of therapy, being correlated with fasting insulin concentration and indices of insulin sensitivity before and after 1 year of therapy. CONCLUSIONS: Children with PWS are characterized by an intact insulin sensitivity with a decrease and a delay of insulin secretion, regardless of moderate obesity or GH treatment. In the present setting, the carbohydrate metabolism is not impaired by GH therapy, but by the excessively increased fat mass.     

Increased insulin sensitivity and maintenance of glucose utilization rates in fetal sheep with placental insufficiency and intrauterine growth restriction

In this study we determined body weight-specific fetal (umbilical) glucose uptake (UGU), utilization (GUR), and production rates (GPR) and insulin action in intrauterine growth-restricted (IUGR) fetal sheep. During basal conditions, UGU from the placenta was 33% lower in IUGR fetuses, but GUR was not different between IUGR and control fetuses. The difference between glucose utilization and UGU rates in the IUGR fetuses demonstrated the presence and rate of fetal GPR (41% of GUR). The mRNA concentrations of the gluconeogenic enzymes glucose-6-phophatase and PEPCK were higher in the livers of IUGR fetuses, perhaps in response to CREB activation, as phosphorylated CREB/total CREB was increased 4.2-fold. A hyperglycemic clamp resulted in similar rates of glucose uptake and utilization in IUGR and control fetuses. The nearly identical GURs in IUGR and control fetuses at both basal and high glucose concentrations occurred at mean plasma insulin concentrations in the IUGR fetuses that were approximately 70% lower than controls, indicating increased insulin sensitivity. Furthermore, under basal conditions, hepatic glycogen content was similar, skeletal muscle glycogen was increased 2.2-fold, the fraction of fetal GUR that was oxidized was 32% lower, and GLUT1 and GLUT4 concentrations in liver and skeletal muscle were the same in IUGR fetuses compared with controls. These results indicate that insulin-responsive fetal tissues (liver and skeletal muscle) adapt to the hypoglycemic-hypoinsulinemic IUGR environment with mechanisms that promote glucose utilization, particularly for glucose storage, including increased insulin action, glucose production, shunting of glucose utilization to glycogen production, and maintenance of glucose transporter concentrations.     

Very low-carbohydrate versus isocaloric high-carbohydrate diet in dietary obese rats

Objective: The effects of a very low‐carbohydrate (VLC), high‐fat (HF) dietary regimen on metabolic syndrome were compared with those of an isocaloric high‐carbohydrate (HC), low‐fat (LF) regimen in dietary obese rats. Research Methods and Procedures: Male Sprague‐Dawley rats, made obese by 8 weeks ad libitum consumption of an HF diet, developed features of the metabolic syndrome vs. lean control (C) rats, including greater visceral, subcutaneous, and hepatic fat masses, elevated plasma cholesterol levels, impaired glucose tolerance, and fasting and post‐load insulin resistance. Half of the obese rats (VLC) were then fed a popular VLC‐HF diet (Weeks 9 and 10 at 5% and Weeks 11 to 14 at 15% carbohydrate), and one‐half (HC) were pair‐fed an HC‐LF diet (Weeks 9 to 14 at 60% carbohydrate). Results: Energy intakes of pair‐fed VLC and HC rats were less than C rats throughout Weeks 9 to 14. Compared with HC rats, VLC rats exhibited impaired insulin and glycemic responses to an intraperitoneal glucose load at Week 10 and lower plasma triacylglycerol levels but retarded loss of hepatic, retroperitoneal, and total body fat at Week 14. VLC, HC, and C rats no longer differed in body weight, plasma cholesterol, glucose tolerance, or fasting insulin resistance at Week 14. Progressive decreases in fasting insulin resistance in obese groups paralleled concomitant reductions in hepatic, retroperitoneal, and total body fat. Discussion: When energy intake was matched, the VLC‐HF diet provided no advantage in weight loss or in improving those components of the metabolic syndrome induced by dietary obesity and may delay loss of hepatic and visceral fat as compared with an HC‐LF diet.     

Ontogeny of the insulin response to glucose in fetal and adult sheep

The purpose of the present experiments was to examine in sheep whether the fetal insulin response to glucose was present by day 110 (d110) of pregnancy and whether the magnitude of the fetal insulin response changed between d110 and d145 (term). We also compared the responses observed in fetuses to those of adult nonpregnant sheep. Basal concentrations of glucose measured in plasma collected from the fetal femoral artery rose progressively between d110 and d145 of gestation, but did not attain the plasma glucose concentrations measured in adult sheep. Peak glucose concentrations in fetuses were achieved 10 min following the bolus injection of glucose (0.8 g/kg estimated fetal body weight) into the fetal femoral vein, and peak values increased with gestational age. Significantly higher peak glucose concentrations were achieved in adult sheep. The concentration of insulin rose rapidly in fetuses at d110, and a similar time course of insulin release in plasma was seen at all gestational ages. The peak plasma insulin concentrations were achieved at 20 min and were significantly greater in older (d140-145) than younger (d125-130) fetuses (p less than 0.05). Peak insulin values in fetuses were much less than in adult sheep. In adult sheep glucose and insulin concentrations remained elevated at 120 min following the injection of glucose, whereas in the fetus the concentration of insulin had returned to preinjection values by 60 min. The insulin/glucose ratio did not change in fetal lambs over the last one third of gestation and was not different from the adult sheep.(ABSTRACT TRUNCATED AT 250 WORDS)     

Occurrence of spontaneous diabetes mellitus in a cynomolgus monkey (Macaca fascicularis) and impaired glucose tolerance in its descendants

Spontaneous diabetes mellitus was diagnosed in a cynomolgus monkey. Clinical and pathological features, such as abnormal glucose tolerance, loss of insulin response, or degeneration of pancreatic beta-cells, resemble human noninsulin-dependent diabetes mellitus. Two descendants of the monkey have developed impaired glucose tolerance and insulin response. Genetic factors seem involved in the appearance of carbohydrate intolerance in this family group of monkeys.     

蛋白质精氨酸甲基化修饰在糖代谢调节中的作用

蛋白质精氨酸甲基化是重要的细胞翻译后修饰方式,参与众多生命过程. 精氨酸的甲基化修饰与糖代谢相关疾病如糖尿病、糖耐量异常密切相关. 蛋白质精氨酸甲基化转移酶(protein arginine methyltransferases, PRMTs)活性下降及表达异常是糖代谢疾病的重要发病基础. 目前研究表明,PRMT1、PRMT4、PRMT5在糖代谢调节中均扮演重要角色,与糖代谢关键酶如磷酸烯醇式丙酮酸羧基激酶、葡萄糖6磷酸酶,胰岛素受体 胰岛素受体配体1 磷脂酰肌醇3激酶通道及其它通路密切相关. 给予甲基化抑制剂MTA及siRNA干扰甲基化则可引发糖代谢紊乱,进而诱发糖代谢疾病. 糖尿病药物罗格列酮、氨基胍与蛋白质精氨酸甲基化也有一定联系. 深入研究蛋白质精氨酸甲基化与糖代谢调节之间的联系及机制,可为防治糖代谢疾病及相关并发症提供更多的理论依据.     

Contribution of defects in glucose uptake to carbohydrate intolerance in liver cirrhosis: assessment during physiological glucose and insulin concentrations

It is well established that subjects with liver cirrhosis are insulin resistant, but the contribution of defects in insulin secretion and/or action to glucose intolerance remains unresolved. Healthy individuals and subjects with liver cirrhosis were studied on two occasions: 1) an oral glucose tolerance test was performed, and 2) insulin secretion was inhibited and glucose was infused in a pattern and amount mimicking the systemic delivery rate of glucose after a carbohydrate meal. Insulin was concurrently infused to mimic a healthy postprandial insulin profile. Postabsorptive glucose concentrations were equal (5.36 +/- 0.12 vs. 5.40 +/- 0.25 mmol/l, P = 0.89), despite higher insulin (P < 0.01), C-peptide (P < 0.01), and free fatty acid (P = 0.05) concentrations in cirrhotic than in control subjects. Endogenous glucose release (EGR; 11.50 +/- 0.50 vs. 11.73 +/- 1.00 mumol.kg(-1).min(-1), P = 0.84) and the contribution of gluconeogenesis to EGR (6.60 +/- 0.47 vs. 6.28 +/- 0.64 mumol.kg(-1).min(-1), P = 0.70) were unaltered by cirrhosis. A minimal model recently developed for the oral glucose tolerance test demonstrated an impaired insulin sensitivity index (P < 0.05), whereas the beta-cell response to glucose was unaltered (P = 0.72). During prandial glucose and insulin infusions, the integrated glycemic response was greater in cirrhotic than in control subjects (P < 0.05). EGR decreased promptly and comparably in both groups, but glucose disappearance was insufficient at the prevailing glucose concentration (P < 0.05). Moreover, identical rates of [3-(3)H]glucose infusion produced higher tracer concentrations in cirrhotic than in control subjects (P < 0.05), implying a defect in glucose uptake. In conclusion, carbohydrate intolerance in liver cirrhosis is determined by insulin resistance and the ability of glucose to stimulate insulin secretion. During prandial glucose and insulin concentrations, EGR suppression was unaltered, but glucose uptake was impaired, which demonstrates that intolerance can be ascribed to a defect in glucose uptake, rather than abnormalities in glucose production or beta-cell function. Although insulin secretion ameliorates glucose intolerance, impaired glucose uptake during physiological glucose and insulin concentrations produces marked and sustained hyperglycemia, despite concurrent abnormalities in glucose production or insulin secretion.     

Effects of chronic N(omega)-nitro-L-arginine methyl ester administration on glucose tolerance and skeletal muscle glucose transport in the rat.

It has been suggested that nitric oxide (NO) is a key regulator of carbohydrate metabolism in skeletal muscle. The present study was undertaken to examine the effects of chronic in vivo competitive antagonism of NO synthase (NOS) by the administration of N(omega)-nitro-L-arginine methyl ester (L-NAME) in the drinking water (1 mg/ml) for 14 days on glucose tolerance and skeletal muscle glucose transport in rats. Oral glucose tolerance tests (OGTT) revealed an impaired glucose tolerance in the L-NAME-treated rats as reflected by the area under the glucose curve (4675 +/- 514 mg% x 120 min (control) vs 6653 +/- 571 mg% x 120 min (L-NAME treated); P < 0.03). While a large rise in plasma insulin concentration was present in the control rats (0.87 +/- 0.34 ng/ml, P < 0.001) during the first 15 min of the OGTT, rises in plasma insulin concentration were absent in the L-NAME-treated rats (0.18 +/- 0.13 ng/ml, P = NS). Intravenous glucose tolerance tests confirmed an impaired insulin secretion in the L-NAME-treated rats. In contrast, insulin-stimulated 2-deoxyglucose transport was enhanced (P < 0.03) by chronic NOS inhibition (5.29 +/- 0.83 nmol/g/min) compared to control rats (2.21 +/- 0.90 nmol/g/min). Plasma sodium concentrations were lower and plasma potassium concentrations were higher in the L-NAME-treated group, indicating an impaired electrolyte status. We conclude that chronic in vivo administration of a NOS inhibitor, while not impairing basal parameters of carbohydrate metabolism, may manifest different responses than acute exposure to the same agent in vitro.     

Hyperglycemic effect of prolactin in anterior pituitary transplanted rats

The role of prolactin as a diabetogenic hormone was based on studies describing the ability of administered prolactin to raise the level of serum glucose. In the present study, female rats were made hyperprolactinemic by the transplantation of two anterior pituitary glands under the renal capsule, obtained from littermate donors. Chronic hyperprolactinemia increased blood glucose and impaired the glycolytic pathway of hepatic carbohydrate metabolism. However, basal serum insulin values were not different from those of controls. These data suggest that chronic hyperprolactinemia has an hyperglycemic effect and has a significant influence on glucose handling by the liver, through reduced glycolysis.     

Maternal and fetal growth, body composition, endocrinology, and metabolic status in undernourished adolescent sheep

The influence of relative maternal undernutrition on growth, endocrinology, and metabolic status in the adolescent ewe and her fetus were investigated at Days 90 and 130 of gestation. Singleton pregnancies to a single sire were established, and thereafter ewes were offered an optimal control (C; n = 14) or low (L [0.7 x C]; n = 21) dietary intake. Seven ewes receiving the L intake were switched to the C intake on Day 90 of gestation (L-C). At Day 90, live weight and adiposity score were reduced (P < 0.001) in L versus C dams. Plasma insulin and IGF1 concentrations were decreased (P < 0.02), whereas glucose concentrations were preserved in L relative to C intake dams. Fetal and placental mass was independent of maternal nutrition at this stage. By Day 130 of gestation, when compared to C and L-C dams, maternal adiposity was further depleted in L intake dams; concentrations of insulin, IGF1, and glucose were reduced; and nonesterified fatty acids increased. At Day 130, placental mass remained independent of maternal nutrition, but body weight was reduced (P < 0.01) in L compared with C fetuses (3555 g vs. 4273 g). Body weight was intermediate (3836 g) in L-C fetuses. Plasma glucose (P < 0.03), insulin (P < 0.07), and total liver glycogen content (P < 0.04) were attenuated in L fetuses. Fetal carcass analyses revealed absolute reductions (P < 0.05) in dry matter, crude protein, and fat, and a relative (g/kg) increase in carcass ash (P < 0.01) in L compared with C fetuses. Thus, limiting maternal intake during adolescent pregnancy gradually depleted maternal body reserves, impaired fetal nutrient supply, and slowed fetal soft tissue growth.     

Effects of S-nitroso-N-acetyl-penicillamine administration on glucose tolerance and plasma levels of insulin and glucagon in the dog.

It has been suggested that nitric oxide (NO, nitrogen monoxide) is a regulator of carbohydrate metabolism in skeletal muscle. The present study was undertaken to investigate the acute effects of the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP) on blood glucose levels and on the gluco-regulatory hormones insulin and glucagon in healthy dogs. The acute effects of SNAP on mean arterial pressure and heart rate were also investigated. The drug was administered intravenously and the pre- and postprandial blood glucose, plasma insulin, and glucagon concentrations were determined at half-hour time intervals postadministration after a glucose challenge. The plasma nitrate and nitrite concentrations were measured and taken as the biochemical markers of in vivo NO formation. The oral glucose tolerance test revealed an impaired glucose tolerance in SNAP-treated dogs as reflected by the area under the glucose curve, 1150.50 +/- 63.00 mmol x 150 min and 1355.25 +/- 102.01 mmol/L x 150 min in dogs treated with 10 and 20 mg/kg of SNAP, respectively, compared with 860.25 +/- 60.68 mmol/L x 150 min in captopril-treated controls (P < 0.05). The 2-h blood glucose concentration in dogs treated with 20 mg/kg body wt of SNAP was 9.17 +/- 1.10 mmol/L compared with 5.59 +/- 0.26 mmol/L for captopril-treated controls (P = 0.015). The oral glucose tolerance test also confirmed an impaired insulin secretion in the SNAP-treated dogs. While the plasma insulin concentration increased gradually in the captopril-treated controls to a peak value of 39.50 +/- 2.55 microIU/ml, 1.5 h after a glucose challenge there was a decrease in the plasma insulin concentration in SNAP-treated dogs to a low value of 20.67 +/- 0.88 microIU/ml (P = 0.006). In contrast, there were no significant differences in plasma glucagon concentration in SNAP-treated dogs and captopril-treated dogs at any time points. Using the Griess reaction, we found that there was a 27-95% increase in plasma nitrate/nitrite concentration on administration of SNAP. The sustained hyperglycemic effect observed in SNAP-treated dogs was accompanied by a marginal decrease in the mean arterial blood pressure and a significant increase in heart rate (P < 0.05). We conclude that acute administration of SNAP in the oral glucose tolerance test releases NO that modulates the parameters of carbohydrate metabolism.     

High levels of dietary carbohydrate increase glucose transport in poult intestine

The hypothesis was proposed that the carbohydrate in the first diet fed to turkey hatchlings upregulates the glucose transport system. Heavy and light body mass poults were observed to determine differences in glucose transport and carbohydrate digestion. Poults were weighed immediately posthatching. Heavy poults were at least +/-2 S.D. above the mean whereas light poults were at least +/-S.D. below the population mean (62.5 +/- 0.4). Each group was randomly assigned to one of two diets. One diet contained 50% carbohydrate and the remaining diet had 15% carbohydrate. Although the diets were isocaloric, differing carbohydrate (corn starch) and fat (cottonseed oil) content had significant effects on body masses within 3 days. Poults fed low carbohydrate weighed more than those on high carbohydrate perhaps because fat is a preferred energy substrate in the neonatal turkey. Greater carbohydrate in the diet increased glucose uptake and maltase activity compared to diets containing more fat. Heavier poults at hatching remained heavier at 3 days posthatching. No differences between body mass categories were noted in glucose uptake measurements. Thus, differences seen in growth rates may not be attributed to glucose transport in the jejunum. It is concluded that turkeys belong to the class of birds in which the poults respond to more carbohydrate in the diet by increasing plasma T(3) concentrations, upregulating the glucose transport system, and increasing enzymatic activity as with maltase.     

Adropin deficiency is associated with increased adiposity and insulin resistance

Adropin is a secreted peptide that improves hepatic steatosis and glucose homeostasis when administered to diet-induced obese mice. It is not clear if adropin is a peptide hormone regulated by signals of metabolic state. Moreover, the significance of a decline in adropin expression with obesity with respect to metabolic disease is also not clear. We investigated the regulation of serum adropin by metabolic status and diet. Serum adropin levels were high in chow-fed conditions and were suppressed by fasting and diet-induced obesity (DIO). High adropin levels were observed in mice fed a high-fat low carbohydrate diet, whereas lower levels were observed in mice fed a low-fat high carbohydrate diet. To investigate the role of adropin deficiency in metabolic homeostasis, we generated adropin knockout mice (AdrKO) on the C57BL/6J background. AdrKO displayed a 50%-increase in increase in adiposity, although food intake and energy expenditure were normal. AdrKO also exhibited dyslipidemia and impaired suppression of endogenous glucose production (EndoR(a)) in hyperinsulinemic-euglycemic clamp conditions, suggesting insulin resistance. While homo- and heterozygous carriers of the null adropin allele exhibited normal DIO relative to controls, impaired glucose tolerance associated with weight gain was more severe in both groups. In summary, adropin is a peptide hormone regulated by fasting and feeding. In fed conditions, adropin levels are regulated dietary macronutrients, and increase with dietary fat content. Adropin is not required for regulating food intake, however, its functions impact on adiposity and are involved in preventing insulin resistance, dyslipidemia, and impaired glucose tolerance.