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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kidney function was studied in six normal males before and during a 2 h glucagon (10 ng/kg/min) infusion. The following variables were determined during each 20 min clearance period; glomerular filtration rate (GFR), renal plasma-flow (RPF) , filtration fraction (FF), urinary albumin and beta2-microglobulin-excretion rates. Glucagon infusion resulted in a fourfold increase in plasma glucagon concentration. The infusion induced a significant increase in GFR (+9%), FF (+9%) and urinary beta2-microglobulin excretion rate (+32%), (p less than 0.01). RPF and urinary albumin excretion rates were not significantly changed. We suggest that glucagon may contribute to the reversible kidney function alterations typically found in poorly regulated juvenile diabetes, a state with relative or absolute hyperglucagonaemia.
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PMID:The effect of short-term glucagon infusion on kidney function in normal man. 33 17

Insulin and glucagon have been studied in 20 subjects (both of the subjects' parents were diabetic or in case of only one diabetic parent, the other showed a first degree familiarity of diabetes): 10 showed normal glucose tolerance ('true prediabetics') and 10 impaired glucose tolerance ('genetic chemical diabetes'). Mean insulin response to oral (100 g) and i.v. glucose load (200 mg/kg followed by 20 mg/kg/min for 60 min) and to arginine infusion (25 g in 30 min) was normal in the prediabetics and delayed and higher in the subjects with chemical diabetes as compared to the control group. Glucagon response to arginine was higher, but not significantly, in prediabetics and in subjects with chemical diabetes. In both of these groups glucagon suppression by glucose was not observed. The insulin/glucagon molar ratio was significantly reduced after glucose infusion in these two groups. No correlation was found between insulin and glucagon secretion after arginine or glucose. A possible alteration in the mechanism controlling glucagon secretion even in the earliest phases of diabetes is suggested.
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PMID:Glucagon and insulin secretion in potential diabetes. 36 Jul 48

A tissue culture-perifusion system is described that allows for long-term culture of pancreatic islets and study of the dynamics of islet hormone secretion. Islets cultured in this system demonstrate brisk, reproducible biphasic insulin and glucagon release. Glucose-stimulated insulin release is similar after 1 or 14 days in culture. Freshly isolated islets are relatively insensitive to somatostatin, requiring 100 ng/ml to suppress partially the glucose-induced insulin secretion. After 24 h of culture, the same islets demonstrate a marked increase in sensitivity to this hormone. Glucagon secretion from islets maintained in this system occurred in a predictable fashion to arginine stimulation and glucose inhibition.
Diabetes 1979 Apr
PMID:Insulin and glucagon secretion from rat islets maintained in a tissue culture-perifusion system. 37 72

The glucagon-secreting A cell is a vital component of the organ system which regulates the distribution of fuel--the islets of Langerhans. Bihormonal control of glucoregulation through a push-pull system maintains the glucose concentration of extracellular fluid within narrow limits irrespective of glucose flux rates through relative equality of glucose influx and efflux. This equality requires appropriate secretion mixtures of the biologic antagonists, insulin and glucagon, directed by a glucose sensor. In severe diabetes, there are virtually no B cells and A cells are in contact largely with other A cells and their glucose-sensing capacity is lost. The A cell hypersecretes and in most juvenile type diabetics aggressive therapy with insulin fails to restore it to normal. Glucagon is a factor in the development of endogenous hyperglycemia, and ketoacidosis. Its suppression may provide a possible approach in the future pharmacologic management of diabetic hyperglycemia.
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PMID:Role of glucagon in diabetes. 40 69

Isologous isolated islets of Langerhans were transplanted into the peritoneum and through the portal vein into the liver of diabetic rats. This resulted in the normalization of fasting blood glucose levels, with clear improvement of glucose tolerance tests. The results after intrahepatic implantation were better than after intraperitoneal implantation. Three months after implantation of islets into the peritoneum diabetes recurred and after one year only 2 of the 15 rats were alive, with high blood glucoe levels. In the group with intrahepatic islets the normalization of blood glucose was maintained over a period of one year. Immunohistochemical insulin proofs were positive in the peritoneum over a period of 3 months and in the liver up to one year after implantation. Glucagon proofs were positive in the intraperitoneal islets for 6 weeks and in intrahepatic ones for one year. Morphological examination of transplanted islets suggested that the liver is better suited for islet transplantation than the peritoneum.
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PMID:Transplantation of isologous islets of Langerhans in diabetic rats. Long-term immunohistochemical results. 41 14

Glucagon immunoreactivity (IRG) was measured in plasma of 8 duodenopancreatectomized patients with antiserum 30-K. Arginine infusions failed to raise plasma IRG, whereas in control subjects IRG rose 3-fold. Column chromatography revealed that the basal IRG measured in these plasmas was not due to glucagon (molecular weight 3485) but to other plasma factors, mainly of high molecular weight. This suggests that diabetes mellitus does not require the presence of glucagon to produce the clinical picture, as suggested by other authors. Plasma levels of the amino acids alanine, serine, ornithine, and arginine were significantly (p less than 0.05) elevated, the former two being gluconeogenic substrates and the latter two constituents of the urea cycle. This amino acid abnormality may be a consequence of glucagon deficiency.
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PMID:[Fractional distribution of anti-glucagon immunoreactivity (GIR) and amino acid concentration in the plasma in duodenopancreatectomized patients; preliminary report]. 43 89

Glucagon secretion before and during arginine infusions was tested in 11 patients with diabetes associated with haemochromatosis. The results were compared with those obtained in six normal subjects and five patients with haemochromatosis but normal glucose tolerance. The patients with haemochromatosis, regardless of glucose tolerance, exhibited higer level of plasma immunoreactivity for glucagon (antiserum 30-K) suggesting hyperglucagonaemia. However, additional analysis revealed that a considerable amount of this glucagon immunoreactivity was due to cross-reacting material of high molecular weight, the levels of which were significantly higher in patients with idiopathic haemochromatosis. When this was deducted from the total immunoreactivity measured, the resulting values for true glucagon concentrations were similar to those of normal subjects. The data suggest that (1) patients with idiopathic haemochromatosis, whether or not associated with diabetes, exhibit plasma glucagon levels comparable with those of normal subjects; (2) the plasma of the same patients contains significantly more high-molecular-weight substances reacting with glucagon antiserum 30-K than is present in plasma of normal subjects; and (3) 'hyperglucagonaemia' may be erroneously suggested when glucagon is measured with certain antisera reputed to be specific for glucagon.
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PMID:Plasma glucagon in diabetes of haemochromatosis: too low or too high? 43 52

Glucagon-like material has been detected by radioimmunoassay in several areas of the canine brain. High concentrations of glucagon-like immunoreactivity (GLI), measured with antibodies directed against the N-terminal region of glucagon, have been found in the hypothalamus, amygdala, and mesencephalon, but a high concentration of immunoreactive glucagon (IRG), measured with antibodies directed against the C-terminal region of glucagon, has been found only in the hypothalamus. The predominant molecular forms of GLI isolated from brain extracts by affinity chromatography are the same as those isolated from gut extracts. The predominant form of IRG in brain extracts is of the same (approximate) molecular weight as pancreatic glucagon.
Diabetes 1979 Jul
PMID:Glucagon-like polypeptides in canine brain. 44 26

Conditions for the isolation of rat hepatocytes that are responsive to insulin with regard to fatty acid synthesis were explored. Cells prepared according to the procedure of Ingebretsen and Wagle require the presence of fetal calf serum for insulin expression. Cells isolated by the Seglen method are the preparation of choice, since they respond to insulin in a simple, well-defined medium and, moreover, show much higher basal rates of fatty acid synthesis. In the latter cells isolated from fed male rats, the rate of fatty acid synthesis, as determined by tritium incorporation from [3H]H2O at 37 degrees C, is enhanced within 30 min after addition of insulin to the incubation medium; with glucagon, it is depressed. In the presence of insulin, the cellular content of malonyl coenzyme A is noticeably increased, whereas the concentrations of pyruvate, lactate, and citrate are not markedly affected. Glucagon, on the other hand, decreases the concentrations of all four intermediates. The activity of acetyl-CoA carboxylase is stimulated and depressed after addition of insulin and glucagon, respectively. In all conditions tested, the activity of acetyl-CoA carboxylase correlates with the rate of fatty acid synthesis, which in turn correlates with the cellular level of malonyl-CoA.
Diabetes 1979 Sep
PMID:Opposite effects of insulin and glucagon in acute hormonal control of hepatic lipogenesis. 46 8

We report a female small for date neonate, who developed transient diabetes mellitus (TDN) five days after birth and required insulin therapy for five weeks. At the onset of the disease, plasma insulin concentration was extremely low. At four weeks of age, after insulin withdrawal, the patient was still hyperglycemic, and basal insulin values assayed over a period of 24 h were mostly inadequate. Glucagon secretion was not suppressed. Growth hormone levels were lower than those of three small for date infants of the same age. At three months of age, the patient was still intolerant to an oral glucose load, insulin secretion remained inadequate while glucagon paradoxically increased 30 min after glucose challenge. The oral glucose tolerance values were in the normal range at six months of age. We conclude that TDN is caused by a transitory defect of insulin secretion, which would also explain the glucagon response as a consequence of insulin deficiency. We found no evidence associating the insulin antagonists observed in our study with the pathogenesis of this illness.
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PMID:[Transient diabetes mellitus in a dystrophic newborn infant]. 71 99


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