cosyntropin and Diabetes-Mellitus

The aim of this study was to investigate the phenotypic parameters and associated factors characterizing the development of glucose intolerance in polycystic ovary syndrome (PCOS). Among the 121 PCOS female subjects from the Mediterranean region, 15.7 and 2.5% displayed impaired glucose tolerance and type 2 diabetes, respectively. These subjects were included in a single group of overweight or obese subjects presenting with glucose intolerance (GI) states. PCOS women with normal glucose tolerance (81.8%) were subdivided into two groups: those who were overweight or obese and those of normal weight. Metabolic and hormonal characteristics of the GI group included significantly higher fasting and glucose-stimulated insulin levels, more severe insulin resistance, hyperandrogenemia, and significantly higher cortisol and androstenedione responses to 1-24 ACTH stimulation. One important finding was that lower birth weight and earlier age of menarche were associated with GI in PCOS women. Frequency of hirsutism, oligomenorrhea, acne, and acanthosis nigricans did not characterize women with GI. Our findings indicate that PCOS patients with GI represent a subgroup with specific clinical and hormonal characteristics. Our observations may have an important impact in preventative and therapeutic strategies.

Topics: Adolescent; Adult; Androstenedione; Blood Glucose; Cohort Studies; Cosyntropin; Diabetes Mellitus; Diabetes Mellitus, Type 2; Family Health; Feeding Behavior; Female; Glucose Intolerance; Humans; Hydrocortisone; Insulin; Insulin Resistance; Mediterranean Region; Obesity; Phenotype; Physical Fitness; Polycystic Ovary Syndrome; Sex Hormone-Binding Globulin

Topics: 17-alpha-Hydroxypregnenolone; 17-alpha-Hydroxyprogesterone; Adrenal Glands; Adult; Aged; Aged, 80 and over; Androgens; Cosyntropin; Dexamethasone; Diabetes Mellitus; Diabetes Mellitus, Type 2; Estrogens; Female; Humans; Hydroxyprogesterones; Male; Middle Aged; Obesity; Premenopause

Patients with diabetes generally exhibit normal plasma catecholamine responses to standing. Some have blunted norepinephrine responses and postural hypotension-hypoadrenergic postural hypotension due to classic diabetic adrenergic neuropathy. Others, including some with postural hypotension, have exaggerated norepinephrine responses to standing. In order to clarify the pathogenesis of this hyperadrenergic state which occurs in a subset of diabetic patients, we studied aldosterone secretion, vascular and metabolic responsiveness to the administration of norepinephrine, and intravascular volumes in four diabetic patients who were selected for their exaggerated plasma norepinephrine responses to standing. Three of the four patients also exhibited (hyperadrenergic) postural hypotension. None of the hyperadrenergic diabetic patients had evidence of hypoaldosteronism or vascular resistance to norepinephrine, but all four patients had subnormal red blood cell masses and the mean (+/-SE) red blood cell mass (13.1 +/- 1.0 ml/kg) was approximately half of that of age- and sex-matched diabetic controls (26.5 +/- 2.7 ml/kg, p less than 0.01). Thus, intravascular volume contraction, specifically a reduction in the red blood cell mass, may play an important role in the pathogenesis of hyperadrenergic state observed in a subset of diabetic patients and in the pathogenesis of hyperadrenergic postural hypotension in affected diabetic patients.

Topics: Acetoacetates; Adult; Aldosterone; Blood Pressure; Cosyntropin; Diabetes Complications; Diabetes Mellitus; Diet, Sodium-Restricted; Epinephrine; Erythrocyte Volume; Female; Glycerol; Humans; Hydrocortisone; Hydroxybutyrates; Hypotension, Orthostatic; Male; Middle Aged; Norepinephrine; Posture; Sympathetic Nervous System