Brain uptake and release of amino acids in nondiabetic and insulin-dependent diabetic subjects: Important role of glutamine release for nitrogen balance

SummaryIn 30 insulin-dependent diabetic patients protein C (PC) antigen and PC activity were significantly lower than those of matched control healthy subjects. An inverse correlation between fasting plasma glucose and both PC concentration and activity was present in diabetics, while a direct correlation between PC concentration and PC activity was observed. Induced hyperglycemia in diabetic and normal subjects was able to decrease both PC antigen levels and PC activity, and heparin reversed in part this effect.In diabetic patients euglycemia obtained by insulin infusion restored to normal the depressed PC levels. Heparin did not alter both the basal PC concentration and activity in healthy controls.These data stress the major role of hyperglycemia in determining PC decrease in diabetics, and suggest that PC reduction is probably associated to hyperglycemia-enhanced thrombin formation.

Download Full-text

Étude des troubles des conduites alimentaires dans une population d'adolescentes souffrant de diabète insulino-dépendant

The Canadian Journal of Psychiatry ◽

10.1177/070674379303800908 ◽

1993 ◽

Vol 38 (9) ◽

pp. 606-610 ◽

Cited By ~ 8

Author(s):

Gilbert Vila ◽

Chantal Nollet-Clemencon ◽

Luis Vera ◽

Héléne Crosnier ◽

Jean-Jacques Robert ◽

...

Keyword(s):

Eating Disorders ◽

Anorexia Nervosa ◽

Adolescent Girls ◽

Glycosylated Hemoglobin ◽

Blood Levels ◽

Dietary Restrictions ◽

Insulin Dependent ◽

Insulin Dependent Diabetic ◽

Restrictive Pattern

The existence of a relationship between Insulin-Dependent Diabetes and eating disorders has recently been observed, but its prevalence and impact on somatic functioning remain poorly understood. These dimensions were evaluated in a population of 52 insulin-dependent diabetic adolescent girls and compared with evaluations of matched subjects from the general population. Results showed that the occurence of anorexia nervosa is rare, the occurence of unspecified eating disorders is frequent (35%) and the occurence of bulimia nervosa is nearly six percent. Poor metabolic control as reflected in blood levels of glycosylated hemoglobin (HBA1C) was found in bulimic subjects and a tendency to be overweight was found in subjects with an unspecified eating disorder. Since such disorders frequently involve dietary restrictions, the role of a restrictive pattern in the occurence of eating disorders is raised.

Download Full-text

Alpha-adrenoceptors and insulin release from pancreatic islets of normal and diabetic rats

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1989.257.3.e439 ◽

1989 ◽

Vol 257 (3) ◽

pp. E439-E443 ◽

Cited By ~ 1

Author(s):

C. G. Ostenson ◽

A. G. Cattaneo ◽

J. C. Doxey ◽

S. Efendic

Keyword(s):

Pancreatic Islets ◽

Insulin Release ◽

Inhibitory Effect ◽

Diabetic Rats ◽

Adrenergic Agonist ◽

Alpha Adrenoceptors ◽

Insulin Dependent ◽

Insulin Dependent Diabetic

The role of alpha-adrenoceptors in the regulation of glucose-induced insulin release (GIR) was investigated in islets of normal and neonatally streptozotocin-injected non-insulin-dependent diabetic rats (STZ). In normal islets GIR was suppressed to approximately 50% by 10(-8) M of the alpha 2-adrenergic agonist UK 14304, whereas 10(-9) M of the agonist induced a similar inhibition in STZ islets. In normal islets, suppression of GIR by UK 14304 (10(-8) M) was totally antagonized by 10(6) M idazoxan (alpha 2-antagonist) or 10(6) M phentolamine (alpha 1 + alpha 2-antagonist). In STZ islets, the inhibitory effect of UK 14304 (10(-9) M) was entirely reversed by 10(-5) M idazoxan or 10(-6) M phentolamine. The alpha 1-antagonist prazosin (10(-7)-10(-5) M) was without effect on insulin release suppressed by UK 14304 in normal and STZ islets. Insulin release at 3.3, 8.3, or 16.7 mM glucose was augmented by phentolamine but not by idazoxan. It is concluded that the inhibitory effect of catecholamines on insulin release is mediated by alpha 2-receptors in normal and STZ islets. Phentolamine augments basal and glucose-induced insulin release by a mechanism that does not involve alpha 2-adrenoceptors.

Download Full-text