BACKGROUND: The aim of the present study was to compare specific causes of death in Type 2 diabetic patients attending and not attending the diabetes center. METHODS: The study was carried out within the framework of the Verona Diabetes Study, a population-based survey of known diabetes prevalence with a 10-year mortality follow-up. On 31 December 1986, 7148 Type 2 diabetic patients were identified in Verona, north-east Italy. Among them 4047 regularly attended the diabetes center, while 3101 did not attend the diabetes center. On 31 December 1996, life status was determined and the underlying cause of death was coded according to the ICD-9. During the follow-up, 2896 subjects died. Difference in mortality from specific causes between attenders and non-attenders were evaluated by a Cox model, controlling for sex, age, diabetes treatment and place of residence (downtown vs suburbs). RESULTS: Mortality was lower in subjects who attended the diabetes center (38. 6% vs 43.0%, p<0.001). This phenomenon was mainly due to lower cardiovascular (p=0.002) and digestive (p=0.047) mortality. CONCLUSIONS: These data support the conclusion that attending the diabetes center reduces cardiovascular and, to a lesser extent, digestive mortality.

Aged↗

PubMedDate not supplied

[Oral carbohydrate tolerance and insulin response in thyrotoxicosis and hypothyroidism].

Explore the source record for details and available documents.

Adult↗

PubMedDate not supplied

[Insulin production in the postgastrectomy hypoglycemic syndrome].

Explore the source record for details and available documents.

Blood Glucose↗

PubMedDate not supplied

Plasma concentrations of glucagon during hyperglycemic clamp with or without somatostatin infusion in obese subjects.

The aim of the present study was to evaluate whether the inhibitory effect on pancreatic A-cell exerted by hyperglycemic hyperinsulinemia and/or by somatostatin administration is impaired in human obesity. For this purpose plasma glucagon concentrations were measured in 8 obese and 8 nonobese nondiabetic subjects during a 4-h hyperglycemic clamp. Synthetic cyclic somatostatin-14 was infused at the rate of 2.5 nmol/min during the third hour of the study. Fasting plasma glucagon was higher in obese than in nonobese subjects (242 +/- 32 vs 163 +/- 15 pg/ml, p less than 0.05) (mean +/- SEM). In the last 20 min of the glucose infusion period preceding somatostatin administration (100-120 min of the study) plasma glucagon averaged 195 +/- 26 pg/ml in obese and 122 +/- 13 pg/ml in nonobese subjects (p less than 0.05), with a reduction of 19 +/- 3% in the former and 28 +/- 4% in the latter (p = n.s.). In both groups somatostatin infusion did not result in a further decrease in plasma glucagon, which averaged 192 +/- 27 pg/ml in obese and 123 +/- 16 pg/ml in nonobese subjects (p less than 0.05) in the 160-180 min period of the study. Also after discontinuing somatostatin infusion plasma glucagon levels did not change. These results suggest that in human obesity hyperglycemic hyperinsulinemia has a normal inhibitory effect on pancreatic A-cell and that somatostatin administration has no additive effect on hyperglycemia and hyperinsulinemia in either obese or nonobese nondiabetic subjects.

Adult↗

PubMedDate not supplied

Glucagon and insulin secretion in potential diabetes.

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.

Adult↗