c-peptide and Hypotension--Orthostatic

Data on the hypokinesia-induced transformation of the glycemic profile and ultrasonic changes in the pancreas structure are presented. The AOH study gave further evidence of transforming glycemic curves. Moreover, increased sizes of tail and head of the pancreas and a decrease in its echogeneity were observed in all test-subjects. Structural changes in the pancreas were confirmed by biochemical investigations which revealed increased levels of blood enzymes and activation of insulin secretion. Increases in the liver size, thickness of the wall of the stomach, diameter of the splenic vein were indicative of progressing venous plethora in the portal vein system. It was shown that venous plethora are the main cause for changes in the upper GI, and in the pancreas state in particular, which can be qualified as dysfunctional. These structural changes in the pancreas could suppress its functional activity manifested by increases in blood enzymes and hormones and transformation of the glycemic profile during the glucose load.

Topics: Adult; Aerospace Medicine; Amylases; C-Peptide; Humans; Hyperglycemia; Hypokinesia; Hypotension, Orthostatic; Insulin; Male; Pancreas; Portal Vein; Space Flight; Ultrasonography

Recombinant human insulin-like growth factor I (rhIGF-I) lowers blood glucose, serum insulin, C-peptide, and lipid levels in healthy and diabetic animals and humans. We hypothesized that rhIGF-I might control blood glucose levels and concomitantly reduce pancreatic insulin secretion in patients with type II diabetes. If true, rhIGF-I might serve as a therapeutic agent that could mitigate some of the detrimental effects of hyperinsulinemia secondary to insulin resistance in these patients. In this study, we treated 12 patients with type II diabetes mellitus twice daily for 5 days with sc rhIGF-I in doses of 90, 120, or 160 micrograms/kg body weight. Metabolic parameters in the fasting and postprandial states were assessed during a 3-day baseline period, the rhIGF-I treatment period, and a 3-day follow-up period, respectively. Administration of rhIGF-I significantly reduced mean (+/- SD) concentrations of fasting blood glucose (12.3 +/- 4.5 to 9.1 +/- 2.6 mmol/L), serum insulin (98 +/- 52 to 56 +/- 27 pmol/L), and C-peptide (993 +/- 298 to 728 +/- 232 pmol/L). It also decreased postprandial (area under the curve) blood glucose (32.5 +/- 12.7 to 23.9 +/- 8.1 mmol/L.h), serum insulin (1102 +/- 707 to 467 +/- 332 pmol/L.h), and C-peptide (5958 +/- 2747 to 3442 +/- 1523 pmol/L.h). The administration of rhIGF-I was also associated with a small but significant reduction in serum triglycerides (6.76 +/- 3.45 to 5.32 +/- 2.59 mmol/L) and total cholesterol (6.13 +/- 1.25 to 5.66 +/- 1.20 mmol/L), 24-h creatinine clearance increased significantly (85 +/- 30 to 133 +/- 51 mL/min), and microalbuminuria was unchanged. Although rhIGF-I was reasonably well tolerated, side effects included low-grade edema, mild and mainly asymptomatic orthostatic hypotension, and bilateral temporomandibular tenderness. We conclude that short-term treatment of type II diabetic patients with rhIGF-I favorably affects metabolic control and enhances kidney function. An assessment of the risk/benefit ratio of rhIGF-I administration to this group of patients awaits extended experiments.

Topics: Aged; Blood Glucose; C-Peptide; Diabetes Mellitus, Type 2; Female; Humans; Hypotension, Orthostatic; Insulin; Insulin-Like Growth Factor I; Kidney; Male; Middle Aged; Recombinant Proteins

The effects of peripheral autonomic neuropathy on the symptomatic, physiological, and hormonal responses to acute insulin-induced hypoglycaemia were studied in two groups of patients with Type 1 diabetes, matched for age, duration of diabetes, and prevailing glycaemic control. A group of eight patients who gave a history of normal awareness of hypoglycaemia and had normal cardiovascular autonomic function tests were compared to a group of six patients who had symptoms of autonomic dysfunction and gross abnormalities of cardiovascular autonomic function tests. An additional two patients with autonomic neuropathy who also had hypoglycaemia unawareness were studied. Acute hypoglycaemia was induced by intravenous infusion of insulin (2.5 mU kg-1 min-1) and the onset of the acute autonomic reaction (R) was identified objectively by the sudden rise in heart rate and onset of sweating. Cognitive function and hypoglycaemia symptom scores were estimated serially, and plasma counterregulatory hormones were measured. Acute autonomic activation was observed to occur in all subjects in response to hypoglycaemia and commenced at similar venous plasma glucose concentrations in both groups (neuropathic patients: 1.6 +/- 0.2 mmol l-1 vs non-neuropathic patients 1.6 +/- 0.2 mmol l-1, p = 0.9,). In the neuropathic patients plasma adrenaline responses were significantly lower at all time points from time R until time R + 30 min (MANOVA for repeated measures, F = 19.4, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Awareness; Blood Glucose; C-Peptide; Cardiovascular System; Cognition; Diabetes Mellitus, Type 1; Diabetic Neuropathies; Diarrhea; Epinephrine; Female; Glucagon; Glycated Hemoglobin; Heart Rate; Humans; Hypoglycemia; Hypotension, Orthostatic; Insulin; Male; Middle Aged; Pancreatic Polypeptide; Reaction Time; Sweating; Valsalva Maneuver