The aim of the present study was to investigate the secretion and hepatic removal of insulin in the healthy offspring of type 2 (non-insulin-dependent) diabetic subjects. For this purpose, we examined the insulin and C-peptide responses to a 75 g oral glucose tolerance test in a group of 55 healthy subjects each having one parent with type 2 diabetes mellitus, and in a group of 55 individuals without a family history of diabetes. All the 110 subjects in the study were ambulatory volunteers, in good general health, and with normal glucose tolerance. The two groups were carefully matched for sex, age, and body weight. Glucose and insulin concentrations as well as incremental areas were similar in the two groups. C-peptide levels and incremental areas were almost identical. C-peptide to insulin molar ratios both in fasting state and after glucose load, as well as relations between C-peptide and insulin incremental areas did not differ in the two groups. In conclusion, the healthy offspring of only one non-insulin-dependent diabetic parent show a normal beta-cell response to glucose, and normal removal of insulin by the liver.
Abstract. A total of 41 patients with hypertension were identified in a survey of 732 healthy factory workers. Twenty‐three of these individuals were receiving antihypertensive medication, whereas 18 cases were newly discovered. Plasma glucose and insulin responses to oral glucose and fasting plasma triglyceride (TG), cholesterol, and high‐density‐lipoprotein (HDL) cholesterol concentrations of these 41 individuals were compared with those of 41 other factor workers, with normal blood pressure, matched with the hypertensive group in terms of gender, age, degree of obesity, job in the factory, and leisure‐time activity. Patients with hypertension had significantly higher plasma glucose ( P < 0.05) and insulin ( P < 0.05) concentrations in response to oral glucose, as well as a higher plasma TG concentration ( P < 0.05). Similar findings were obtained when the treated and untreated hypertensive groups were analysed separately and compared with their respective control groups. However, there were no differences between the treated and untreated hypertensive groups. Ninety per cent of the normotensive group had a plasma insulin concentration of < 500 pmol l −1 2 h after the glucose load. Using this value as the criterion for definition of hyperinsulinaemia, 41% of the patients with high blood pressure were hyperinsulinaemic. In addition to meeting this cut‐off point, the patients with hypertension and hyperinsulinaemia were also glucose intolerant and dyslipidaemic. In conclusion, approximately 50% of an unselected group of patients with hypertension were hyperinsulinaemic. Insulin levels were comparable in treated and untreated patients with high blood pressure, and hyperinsulinaemic patients also tended to be glucose intolerant and dyslipidaemic.
To identify the predictive value on time to onset of heart failure (HF) or cardiac death of clinical, radiographic, and echocardiographic variables, as well as cardiac biomarkers N-terminal pro brain natriuretic peptide (NT-proBNP) and cardiac troponin I in dogs with preclinical myxomatous mitral valve disease (MMVD). One hundred sixty-eight dogs with preclinical MMVD and left atrium to aortic root ratio ≥1.6 (LA:Ao) and normalized left ventricular end-diastolic diameter ≥1.7 were included. Prospective, randomized, multicenter, single-blinded, placebo-controlled study. Clinical, radiographic, echocardiographic variables and plasma cardiac biomarkers concentrations were compared at different time points. Using receiving operating curves analysis, best cutoff for selected variables was identified and the risk to develop the study endpoint at six-month intervals was calculated. Left atrial to aortic root ratio >2.1 (hazard ratio [HR] 3.2, 95% confidence interval [95% CI] 1.9–5.6), normalized left ventricular end-diastolic diameter > 1.9 (HR: 6.3; 95% CI: 3.3–11.8), early transmitral peak velocity (E peak) > 1 m/sec (HR: 3.9; 95% CI: 2.3–6.7), and NT-proBNP > 1500 ρmol/L (HR: 5.7; 95% CI: 3.3–9.5) were associated with increased risk of HF or cardiac death. The best fit model to predict the risk to reach the endpoint was represented by the plasma NT-proBNP concentrations adjusted for LA:Ao and E peak. Logistic and survival models including echocardiographic variables and NT-proBNP can be used to identify dogs with preclinical MMVD at higher risk to develop HF or cardiac death.
The aim of this study was to address the intriguing issue of the role of the insulin-like growth factor (IGF)-1 system in longevity looking at the role of different components of IGF system. Vital status was ascertained in 1,197 men and women aged greater than or equal to 65 years from the InCHIANTI study. Hormonal levels were categorized into quartiles, and ratio of IGF-1 to IGF-binding protein (IGFBP)-1 was calculated. The relationship between hormones and mortality was tested by Cox proportional hazard models adjusted for age, sex, and confounders. During the 8-year follow-up period, 240 died and 957 survived. Lowest quartiles of IGF-1 and IGFBP-1 were considered as reference. Compared with the lowest quartiles, IGF-1 in upper quartiles was a negative predictor of mortality independent of age and sex (p = .01) but not independent of IGFBP-1 and other confounders. IGFBP-1 in second-third quartiles was negatively associated and that in the fourth quartiles was positively associated with risk of death. IGF-1/IGFBP-1 ratio in the lowest quartiles was a strong positive predictor of mortality, in age- and sex-adjusted model (p = .005), and independent of additional confounders (p = .037). High IGFBP-1 and low IGF-1/IGFBP-1 ratio are associated with all-cause mortality in older population.
Administration of pyridoxine-alpha-ketoglutarate (PAK) to a group of insulin-independent non-ketotic diabetics decreased (p less than 0.01) the plasma concentration of lactate response to isometric exercise. The mechanism of action of PAK could be interpreted as a consequence of changes induced by the drug on the Krebs' cycle with a subsequent reduction of lactate production.