Immunoreactive glucagon (IRG) fractions from plasma of 8 normal subjects and 4 patients with glucagon secreting tumors were studied by gel filtration techniques on Bio Gel P--30 and Sephadex G--50 columns. The pancreatic glucagon specific anti serum (30K) of Unger was utilized to measure IRG. Columns were calibrated with labelled albumin, proinsulin, insulin and glucagon. Four peaks were defined in normal and tumor bearing patients: peak I (greater than 20 000 mol. wt.), peak II (primarily 9000 mol. wt.), peak III pancreatic glucagon (3500 mol. wt.) and peak IV small gucagon (less than 3500 mol. wt.). Glucagonoma patients differed from our normal and reported normal subjects in that peak II contained most of the circulating IRG. The percent of IRG associated with peak II was 9.5--31.5% in normals and 39.1--61.2% in glucagonomas. Glucagon-like biological activity in an isolated hepatocyte system was demonstrated for all peaks. However, relative to immunoreactivity, peak II showed reduced activity (25--33%). Immunoassay of dilutions of all peaks revealed the probability of immuno determinants identical with procine pancreatic glucagon. The presence of heterogenous IRG peaks with biological glucagon-like activity suggest that the larger molecules may be prohormones. Further, it is possible that specific elevation of peak II may be a diagnostic feature of glucagonomas.
Mice homozygous and heterozygous for the diabetes (db) gene were studied to determine: 1. whether latent carbohydrate intolerance is present in young normoglycemic diabetic mutants (db/db); 2. whether normoglycemic food restricted diabetic mutants are carbohydrate intolerant; and 3. whether mice heterozygous for the db gene (db/-~) manifest abnormalities in glucose tolerance, serum IRI levels or body weights. Blood glucose levels were determined 0, 1/2, i, 2 and 3 h following intraperitoneal administration of 2 mg glucose/g body weight.Normals (~-/-~) and diabetics (db/db) showed similar glucose tolerance curves during the first two weeks of life ; however, both were markedly glucose intolerant compared to normal adult mice. At 3 weeks a small number of mutants had higher 3 h levels than any achieved in normal mice. By 4 weeks the average value for diabetics prior to glucose loading (0 time) was significantly (P < 0.02) elevated (db/db ~-144 mg glucose/100 ml, -~/-[-~ 124 nag glucose/100 ml). Although food restriction reduced blood glucose concentration at 0 time, persistence of carbohydrate intolerance was readily demonstrable following glucose loading. --Abnormalities in heterozygotes (db/~-), 3 to 16 months of age, were primarily restricted to male mice, which showed moderate, but statistically significant elevations in blood glucose both at 0 time and following glucose administration. Forty percent of male heterozygores had higher serum IRI levels than any observed in normal control males. Body weights of male heterozygotes were significantly greater (P<0.01) than those in agematched normals. Etudes de la ~t~utation dbdb chez la souris: V. Tolgrance au glucose dctns la souris homozygote et hdtgrozygote pour le g~ne diabetique (db)Rdsumg. Des souris homozygotes et h6t@rozygotes porteurs du g~ne du diabbte (db) out 6t6 6tudi6es dans le but de d@terminer: 1. si une intol6rance latente aux hydrates de earbone existe ehez la jeune souris dbdb normo-glyc6mique, 2. si la souris dbdb normoglyc6mique ayant une alimentation r6dnite pr6sente une intol6ranee aux hydrates de carbone, et 3. si la souris h6t6rozygote pour le g~ne db (db/~-) montre des anomalies de la tol6ranee au glucose, des taux d'IRI s6riques et du poids eorporel. Les taux de glucose sanguin out 6t6 mesur6s 0, 30, 60, 120 et 180 rain aprbs l'injeetion intrap@riton6ale de 2 mg glucose/ gramme de poids corporel. Les souris normales (+/~-) et diab6tiques (db/db) ont des courbes de tol6ranee au glucose semblables au cours des 2 premieres semaines de leur vie. I1 appara~t pourtant qu'elles manifestent une intolerance marqu6e an glucose si on les compare avee la souris normale adulte. Un petit nombre de souris db/db ag6es de 3 semaines pr6sentent des glyc6mies plus 61ev6es que celles observ6es ehez les souris normales ~ la 180~me minute du test. A 4 semaines, la glyc6mie moyenne avant la charge glueos@e (0 rain) est significativement plus 61ev6e (P < 0.02) chez les animaux diab6tiques db/db (144 nag glucose %) que chez la souris normale +/+ (124 mg glucose ~o)...
Glucose-induced insulin release was studied in vitro with isolated islets of Langerhans obtained from obese hyperglycemic C57Bl/6J-ob/ob (ob/ob) and lean C57Bl/6J-+/+ (control) mice. The threshold concentrations of glucose for insulin release were determined. In addition, the effect of total fast and of chronic food restriction on in vitro insulin release were studied. The following was observed: 1) with fasting, islet volume decreased. Islets obtained from ob/ob mice were larger than control islets, except for the chronic food restricted group. 2) Ob/ob islets were more sensitive to glucose than were controls in that the threshold for glucose-induced insulin release occured at lower glucose concentrations. 3) Fasting for 48 h completely abolished glucose-induced insulin release in control islets, whereas glucose-induced insulin release was maintained in 48-h and 7-day fasted ob/ob islets. 4) The increased glucose sensitivity of the ob/ob islets was maintained despite chronic food restriction.
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