Effects of dietary soy or urea nitrogen and feeding frequency on nitrogen metabolism, glucose metabolism and urinary metabolite excretion in sheep.
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Animal Feed↗
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Results for “GLUCOSE METABOLISM”
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Effect of pregnancy on glucose metabolism in glucose intolerant 'BB' Wistar rats.
Little is known about the effect of pregnancy on the 'BB' Wistar rat, an animal model of insulin-dependent (type I) diabetes. The pathogenesis of diabetes in this animal model seems to result from antibody-mediated natural killer cell destruction of pancreatic beta cells. The glucose metabolism of glucose intolerant female rats (study group) was studied prior to pregnancy, during pregnancy, and postpartum using glucose tolerance tests (GTT). Control rats with normal GTT were studied and bred in a fashion similar to the study animals. Before becoming pregnant, the GTT levels of the chemically diabetic rats were significantly different from those of the controls (p less than 0.05). The GTT values of the study animals decreased during pregnancy to levels seen in pregnant controls. After pregnancy, the GTT values of the study animals returned to prepregnant levels. Based on these observations, it appears that pregnancy may block the autoimmune destruction of beta cells, causing an increase in insulin production and release, thereby improving glucose metabolism.
Animals↗
Effects of type 2 diabetes on the regulation of hepatic glucose metabolism.
Glucose production is inappropriately increased in people with type 2 diabetes both before and after food ingestion. Excessive postprandial glucose production occurs in the presence of decreased and delayed insulin secretion and lack of suppression of glucagon release. These abnormalities in hormone secretion, coupled with impaired insulin-induced suppression of glucose production and stimulation of splanchnic glucose uptake, likely account in large part for the excessive amounts of glucose that reach the systemic circulation for disposal by peripheral tissues following food ingestion. In contrast, when adequate basal insulin concentrations are present, neither glucagon-induced stimulation of glucose production nor glucose-induced suppression of glucose production differs in diabetic and nondiabetic subjects matched for gender, age, and degree of obesity. However, when insulin secretion is defective, lack of suppression of glucagon can cause substantial hyperglycemia by enhancing rates of glucose production. Therefore, normalization of hepatic glucose metabolism in people with type 2 diabetes mellitus likely will require normalization of insulin and glucagon secretion as well as hepatic insulin action.
Diabetes Mellitus, Type 2↗
Exercise-induced increase in glandular kallikrein activity in human plasma and its significance in peripheral glucose metabolism.
Glucose uptake into skeletal muscle of human forearm at rest and during exercise is reported to be diminished by the administration of a kallikrein (kallidinogenase) inhibitor. The present study was conducted to clarify the changes of glandular kallikrein (GK) activity in human plasma during acute exercise and its significance in peripheral glucose metabolism. 10 non-diabetic inpatients, aged 49.5 years, and 8 diabetic inpatients, aged 53.8 years, were studied. After an overnight fast, bicycle ergometer exercise test was performed for 15 min (25 W (5 min)----50 W (5 min)----75 W (5 min]. Before (basal), during (at 15 min) and after exercise (at 25 min), venous blood samples were drawn to determine plasma GK activity and glucose, serum immunoreactive insulin (IRI), C-peptide immunoreactivity (CPR), nonesterified fatty acids, pyruvate, lactate, noradrenaline and adrenaline levels. In the 1st trial, in both non-diabetics (n = 10) and diabetics (n = 8), plasma GK activity increased significantly during exercise. After the 1st trial, in 6 patients (5 non-diabetics; 1 diabetic), exercise test was repeated once after 2-4 weeks and in a diabetic patient, exercise test was repeated twice at 4-week intervals, accordingly exercise test was performed 26 times in 18 patients in total. Natural logarithmic correlation between sigma glucose level and sigma GK activity (r = 0.52, n = 26), and hyperbolic correlation between sigma glucose level and sigma IRI level (r = -0.66, n = 26) but no correlation between sigma glucose level and sigma CPR level (r = 0.17, n = 26) were found.(ABSTRACT TRUNCATED AT 250 WORDS)
Blood Glucose↗
Clinical research of glucose metabolism.
Glucose metabolism in diabetes and in hypoglycemic states has been studied at IIIrd Medical Department for more than 30 years. The research is now concentrated on the evaluation of insulin action on receptor and postreceptor levels and in biochemical changes accompanying early stages of diabetic microangiopathy. The changes of insulin action has been examined by using the clamp techniques also in patients with organic hyperinsulinism. We study molecular changes of insulin action and pathogenesis of vascular complications.
Diabetes Mellitus↗
Effects of growth hormone on glucose metabolism and glucose transport in 3T3-F442A cells: dependence on cell differentiation.
In differentiated adipocytes of the 3T3-F442A cell line, 4-h incubation with human GH transiently stimulates glucose oxidation and lipid accumulation. When the incubation is extended to 48 h, hGH suppresses these indicators of glucose metabolism. The stimulation of glucose oxidation or lipid accumulation required a period of serum deprivation before incubation with GH, while the later inhibitory effect of GH occurred equally well whether or not cells were serum-deprived. Since the 3T3-F442A adipocytes differentiate in culture from preadipocyte fibroblasts, we examined the importance of the state of differentiation on metabolic responses to GH. GH had no reproducible effect on glucose oxidation after 4 or 48 h in the preadipocyte fibroblasts. To determine whether the effects of GH on glucose metabolism involved changes in glucose transport, the uptake of a low concentration (558 nM) of [14C]glucose was measured in the adipocytes. Glucose uptake increased 2- to 4-fold after 5-15 min of incubation with GH. This rapid response peaked in 15-30 min and subsided by 120 min despite the continued presence of GH. After 24 h of incubation with GH, glucose uptake was inhibited. In preadipocytes, GH occasionally stimulated glucose uptake in a transient manner. When present, the stimulation was generally of lesser magnitude and shorter duration than in the adipocytes. No inhibition of glucose uptake was observed in the preadipocytes after 24 h of incubation. These differences in responsiveness of the preadipocytes compared to the adipocytes cannot be attributed to differences in receptor binding or detectable differences in GH receptor type or size, as determined by migration of [125I]iodohuman GH-receptor complexes in electrophoretic gels. These findings indicate that GH rapidly alters glucose uptake in 3T3-F442A adipocytes. The changes in glucose uptake most likely play a major role in the GH-induced changes in the conversion of glucose to lipid and CO2 observed previously. These metabolic responses to GH are dependent on the adipose conversion of the 3T3-F442A cells. As the 3T3-F442A cells express the adipocyte phenotype, development of increased metabolic regulation by GH appears to require changes in postbinding or postreceptor phenomena.
Adipose Tissue↗
Transfection of AtT-20ins cells with GLUT-2 but not GLUT-1 confers glucose-stimulated insulin secretion. Relationship to glucose metabolism.
Glucose is thought to stimulate insulin release from islet beta-cells through generation of metabolic signals. In the current study we have introduced the genes encoding the facilitated glucose transporters known as GLUT-1 and GLUT-2 into AtT-20ins cells to assess their impact on glucose-stimulated insulin release and glucose metabolism. We find that transfection of AtT-20ins cells with GLUT-2, but not GLUT-1, confers glucose-stimulated insulin release in both static incubation and perifusion studies. Cells transfected with GLUT-1 have a Km for 3-O-methyl glucose uptake of 4 mM and a Vmax of 5-6 mmol/min/liter cell space. These values are increased compared to untransfected AtT-20ins cells (Km = 2 mM; Vmax = 0.5 mmol/min/liter cell space), but are less than observed in GLUT-2-transfected lines (Km = 16-17 mM; Vmax = 17-25 mmol/min/liter cell space). Despite these dramatic differences in glucose transport affinity and capacity, the rates of [5-3H]glucose usage are not different in the control and transfected lines over a range of glucose concentrations from 10 microM to 20 mM. We conclude that the specific effect of GLUT-2 on glucose-stimulated insulin release in AtT-20ins cells is not related to changes in the overall rate of glucose metabolism and may instead involve physical coupling of GLUT-2 with cellular proteins and/or structures involved in glucose signaling.
3-O-Methylglucose↗
Effects of electric stress on glucose metabolism, glucose-stimulated cyclic adenosine 3',5'-monophosphate accumulation and 45 Ca++ efflux in isolated pancreatic islets from rats fed with a high fat diet.
The effects of the electric stress on glucose oxidation, cyclic adenosine 3', 5'-monophosphate (AMP) accumulation and 45Ca++ efflux in response to glucose were studied in pancreatic islets isolated from rats fed on a control (C) or a high fat diet (F) for 12 weeks. The half of rats on each diet were subjected to electrical shocks in the random time schedule for 1 hr per day for the last 3 weeks of the feeding period (group C-S and F-S). The remaining rats were not given any shocks (group C-NS and F-NS). The rats in F-S group had the high levels of plasma epinephrine, dopamine and blood glucose. The basal content of cyclic AMP after 20 min of incubation with 2.8 mM glucose was decreased in islets from F-S group without affecting insulin release. After 20 min of incubation with 25 mM glucose, the cyclic AMP content in islets from F-S group, which was identical with that in F-NS group, was only 50% of that in C-S group. Insulin release in response to high glucose was significantly inhibited in islets from F-S group. In spite of a remarkable increase of cyclic AMP content in islets from C-S group, insulin release did not differ from that in C-NS group. Glucose (16.7 mM)-stimulated 45Ca++ efflux from the perfused islets was greatly inhibited by the high fat diet rather than by stress. The rate of glucose oxidation with 16.7 mM glucose was decreased in islets from F-S group. It is suggested that the decreased insulin release in response to glucose provoked by the combined effects of the feeding of a high fat diet and electric stress may be mediated by changes of the adenylate cyclase-cyclic AMP system on the plasma membrane of the B-cell or be related to changes in glucose metabolism in islets.
Adrenal Cortex↗
Estimating glucose metabolism using glucose analogs and two tracer kinetic models in isolated rabbit heart.
The purpose of this investigation was to 1) evaluate the relative accuracy of the Sokoloff and Patlak tracer kinetic models in estimating glucose metabolic rate (GMR) in the presence and absence of insulin; 2) evaluate the effect of nutritional state on the lumped constant (LC); and 3) compare the kinetics of 2-fluoro-2-deoxy-D-[14C]glucose (FDG) and 2-deoxy-D-[3H]glucose (DG) membrane transport and phosphorylation. The experimental preparation was the isolated, red blood cell-albumin-perfused rabbit heart. Our results showed that both tracer kinetic models provided GMR estimates that correlated well with the Fick method (for FDG, R = 0. 84 and 0.91 for the Sokoloff and Patlak models, respectively); nutritional state did not affect the LC; and FDG and DG have different transport and/or phosphorylation parameters. We also observed that 1) the addition of a fourth compartment to the Sokoloff model reduced the mean squared error between measured and modeled data by a factor of 7.4; 2) a longer time (21.8 min) was required to obtain a linear phase of the Patlak plot than is allowed in clinical studies; and 3) accurate GMR estimates were obtained only by using different LCs reflecting insulin's presence or absence. Our results indicate potential sources of error in the use of FDG and positron emission tomography to quantify GMR in patients.
Animals↗
Abnormal renal, hepatic, and muscle glucose metabolism following glucose ingestion in type 2 diabetes.
Recent studies indicate an important role of the kidney in postprandial glucose homeostasis in normal humans. To determine its role in the abnormal postprandial glucose metabolism in type 2 diabetes mellitus (T2DM), we used a combination of the dual-isotope technique and net balance measurements across kidney and skeletal muscle in 10 subjects with T2DM and 10 age-, weight-, and sex-matched nondiabetic volunteers after ingestion of 75 g of glucose. Over the 4.5-h postprandial period, diabetic subjects had increased mean blood glucose levels (14.1 +/- 1.1 vs. 6.2 +/- 0.2 mM, P < 0.001) and increased systemic glucose appearance (100.0 +/- 6.3 vs. 70.0 +/- 3.3 g, P < 0.001). The latter was mainly due to approximately 23 g greater endogenous glucose release (39.8 +/- 5.9 vs. 17.0 +/- 1.8 g, P < 0.002), since systemic appearance of the ingested glucose was increased by only approximately 7 g (60.2 +/- 1.4 vs. 53.0 +/- 2.2 g, P < 0.02). Approximately 40% of the diabetic subjects' increased endogenous glucose release was due to increased renal glucose release (19.6 +/- 3.1 vs. 10.6 +/- 2.4 g, P < 0.05). Postprandial systemic tissue glucose uptake was also increased in the diabetic subjects (82.3 +/- 4.7 vs. 69.8 +/- 3.5 g, P < 0.05), and its distribution was altered; renal glucose uptake was increased (21.0 +/- 3.5 vs. 9.8 +/- 2.3 g, P < 0.03), whereas muscle glucose uptake was normal (18.5 +/- 1.8 vs. 25.9 +/- 3.3 g, P = 0.16). We conclude that, in T2DM, 1) both liver and kidney contribute to postprandial overproduction of glucose, and 2) postprandial renal glucose uptake is increased, resulting in a shift in the relative importance of muscle and kidney for glucose disposal. The latter may provide an explanation for the renal glycogen accumulation characteristic of diabetes mellitus as well as a mechanism by which hyperglycemia may lead to diabetic nephropathy.
Administration, Oral↗
[Cerebral blood flow, cerebral oxygen metabolism, cerebral glucose metabolism, and tissue pH in human acute cerebral infarction using positron emission tomography].
It is necessary for treatment and deciding prognosis to make clear about changes of cerebral blood flow and metabolism in acute cerebral infarction. This preliminary PET study was designed to investigate physiological and biochemical changes in acute cerebral infarction by positron emission tomography (PET). PET studies were performed in six patients with acute cerebral infarction within 48 hours after onset of stroke using continuous inhalation of C15O2 for cerebral blood flow (CBF), 15O2 for cerebral metabolic rate for oxygen (CMRO2), 11CO for cerebral blood volume, the intravenous injection of 11C-dimethyloxazolidinedione for tissue pH and the intravenous injection of 18F-fluorodeoxyglucose for cerebral metabolic rate for glucose (CMRGlu). Metabolic coupling index (MCI) image was made from CBF image and CMRGlu image to investigate relation between CBF and CMRGlu. Also oxygen glucose index (OGI) image was made from CMRO2 image and CMRGlu image to investigate relation between CMRO2 and CMRGlu. Preliminary results demonstrate that reduction of CBF, CMRO2, and CMRGlu in the affected cortex except for reperfusion case. Increase of OER was recognized four of six cases. Patterns of MCI and OGI in the cortex which CMRO2 value is less than 65 mumol/100 g/min were different from those in the cortex which CMRO2 value is more than 65. MCI of the affected cortex (CMRO2 less than 65) decreased relative to that of the cortex (CMRO2 greater than or equal to 65). OGI of the affected cortex (CMRO2 less than 65) significantly decreased in comparison with that of the cortex (CMRO2 greater than or equal to 65).(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Fetal transplantation following spinal contusion injury results in chronic alterations in CNS glucose metabolism.
Glucose utilization of the injured rat spinal cord was determined using the autoradiographic technique of Sokoloff et al. (33). Animals were analyzed chronically (2 and 3 months) after spinal contusion injury alone or when a spinal lesion was followed by subchronic (10-day) intraparenchymal fetal spinal transplantation. At 2 and 3 months postinjury, spinal glucose utilization was reduced in dorsal gray and white matter above and below the lesion site. In addition, sensory regions of the forebrain and brain stem (e.g., nucleus gracilis and ventral posterior medial nucleus of the thalamus) had a lower basal metabolic rate than control animals. Decreased metabolic rates in supraspinal regions were reversed by the presence of a spinal graft at 3 but not at 2 months postinjury. Furthermore, gray matter in animals receiving an intraspinal transplant had elevated glucose utilization rates for several spinal segments rostral and caudal to the lesion epicenter. Graft glucose utilization was higher at 2 months (80-90 mumol/100 g/min) than at 3 months (60-70 mumol/100 g/min) posttransplantation. These data are the first quantitative metabolic imaging of spinal and brain metabolism following spinal contusion injury and fetal transplantation. The study suggests that intraspinal transplants can become functionally integrated with adjacent host gray matter and can chronically alter specific postinjury metabolic patterns.
Animals↗
Effects of age and sex on postprandial glucose metabolism: differences in glucose turnover, insulin secretion, insulin action, and hepatic insulin extraction.
To determine the effects of age and sex on the regulation of postprandial glucose metabolism, glucose turnover, insulin secretion, insulin action, and hepatic insulin extraction were concurrently measured in 145 healthy elderly (aged 70 +/- 1 years) and in 58 young (aged 28 +/- 1 years) men and women before and after ingestion of a mixed meal containing [1-(13)C]glucose. At the time of meal ingestion, [6-(3)H]glucose and [6,6-(2)H(2)]glucose were infused intravenously to enable concurrent measurement of the rates of postprandial endogenous glucose production (EGP), meal appearance, and glucose disappearance. Fasting and postprandial glucose concentrations were higher (P < 0.001) in both elderly women and elderly men compared with young individuals of the same sex. The higher postprandial glucose concentrations in the elderly than young women were caused by higher rates of meal appearance (P < 0.01) and slightly lower (P < 0.05) rates of glucose disappearance immediately after eating. In contrast, higher glucose concentrations in the elderly than young men were solely due to decreased (P < 0.001) glucose disappearance. Although postprandial glucose concentrations did not differ in elderly women and elderly men, rates of meal appearance and glucose disappearance rates both were higher (P < 0.001) in the women. Fasting EGP was higher (P < 0.05) in elderly than young subjects of both sexes and in women than men regardless of age. On the other hand, postprandial suppression of EGP was rapid all groups. Insulin action and secretion were lower (P < 0.001) in the elderly than young men but did not differ in the elderly and young women. This resulted in lower (P < 0.001) meal disposition indexes in elderly than young men but no difference in elderly and young women. Total meal disposition indexes were lower (P < 0.05) in elderly men than elderly women, indicating impaired insulin secretion, whereas disposition indexes were higher (P < 0.05) in young men than young women. Hepatic insulin clearance was greater (P < 0.001) in the elderly than young subjects of both sexes but did not differ between men and women regardless of age. In contrast, the ability of glucose to facilitate its own uptake (glucose effectiveness) was higher (P < 0.001) in women than men but did not differ in elderly and young subjects. Thus, age and sex impact on insulin secretion, insulin action, hepatic insulin extraction, and glucose effectiveness, resulting in substantial differences in the regulation of postprandial glucose metabolism in men and women and in elderly and young subjects.
Adult↗
The CREB coactivator TORC2 is a key regulator of fasting glucose metabolism.
Glucose homeostasis is regulated systemically by hormones such as insulin and glucagon, and at the cellular level by energy status. Glucagon enhances glucose output from the liver during fasting by stimulating the transcription of gluconeogenic genes via the cyclic AMP-inducible factor CREB (CRE binding protein). When cellular ATP levels are low, however, the energy-sensing kinase AMPK inhibits hepatic gluconeogenesis through an unknown mechanism. Here we show that hormonal and energy-sensing pathways converge on the coactivator TORC2 (transducer of regulated CREB activity 2) to modulate glucose output. Sequestered in the cytoplasm under feeding conditions, TORC2 is dephosphorylated and transported to the nucleus where it enhances CREB-dependent transcription in response to fasting stimuli. Conversely, signals that activate AMPK attenuate the gluconeogenic programme by promoting TORC2 phosphorylation and blocking its nuclear accumulation. Individuals with type 2 diabetes often exhibit fasting hyperglycaemia due to elevated gluconeogenesis; compounds that enhance TORC2 phosphorylation may offer therapeutic benefits in this setting.
AMP-Activated Protein Kinases↗
Hormonal control of glucose metabolism.
Glucose homeostasis is accomplished through two major hormones, glucagon and insulin. These hormones, of course, must work in concert with other permissive hormones such as glucocorticoids and catecholamines to bring about a multiplicity of physiological processes such as gluconeogenesis, glycolysis, lipolysis, and proteolysis that maintain the organism's biochemical integrity.
Blood Glucose↗
Compartment analysis of cerebral glucose metabolism and in vitro glucose-metabolizing enzyme activities in the rat brain.
To clarify the relationship between cerebral glucose metabolic rate constants and glucose-metabolizing enzyme activities in the cerebral cortex, we evaluated the cerebral metabolic rate of glucose (CMRGlu), metabolic rate constants of [18F]-2-fluoro-2-deoxy-D-glucose (FDG) and related enzyme activities in the frontal cortex under normal and glucose metabolism-suppressed conditions. Applying a three-compartment four-parameter model, metabolic rate constants were obtained by dynamic positron emission tomography with FDG, and CMRGlu was calculated based on these rate constants. The glycolytic enzyme activities were determined by in vitro biochemical assay. Three days after ibotenic acid injection into the basal forebrain, CMRGlu was decreased in the ibotenic acid-treated frontal cortex as well as k3* (phosphorylation), while K1* (plasma to brain) showed no remarkable change. No significant reductions of the enzyme activities except for hexokinase activity were found in the frontal cortex. Regression analysis showed a significant positive correlation between k3* and the hexokinase activity. These results suggested that k3* in the compartment analysis reflects hexokinase activity.
Analysis of Variance↗
Regulation of exogenous and endogenous glucose metabolism by insulin and acetoacetate in the isolated working rat heart. A three tracer study of glycolysis, glycogen metabolism, and glucose oxidation.
Myocardial glucose use is regulated by competing substrates and hormonal influences. However, the interactions of these effectors on the metabolism of exogenous glucose and glucose derived from endogenous glycogen are not completely understood. In order to determine changes in exogenous glucose uptake, glucose oxidation, and glycogen enrichment, hearts were perfused with glucose (5 mM) either alone, or glucose plus insulin (40 microU/ml), glucose plus acetoacetate (5 mM), or glucose plus insulin and acetoacetate, using a three tracer (3H, 14C, and 13C) technique. Insulin-stimulated glucose uptake and lactate production in the absence of acetoacetate, while acetoacetate inhibited the uptake of glucose and the oxidation of both exogenous glucose and endogenous carbohydrate. Depending on the metabolic conditions, the contribution of glycogen to carbohydrate metabolism varied from 20-60%. The addition of acetoacetate or insulin increased the incorporation of exogenous glucose into glycogen twofold, and the combination of the two had additive effects on the incorporation of glucose into glycogen. In contrast, the glycogen content was similar for the three groups. The increased incorporation of glucose in glycogen without a significant change in the glycogen content in hearts perfused with glucose, acetoacetate, and insulin suggests increased glycogen turnover. We conclude that insulin and acetoacetate regulate the incorporation of glucose into glycogen as well as the relative contributions of exogenous glucose and endogenous carbohydrate to myocardial energy metabolism by different mechanisms.
Acetoacetates↗
ARE THYROID HORMONES DIABETOGENIC?A STUDY OF PERIPHERAL GLUCOSE METABOLISM DURING GLUCOSE INFUSIONS IN NORMAL SUBJECTS AND HYPERTHYROID PATIENTS BEFORE AND AFTER TREATMENT.
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Adipose Tissue↗