Biomedical subjects

A Golay

Publications and source records attributed to A Golay.

130 records · Page 8Linked to original sources

PubMedDate not supplied

[Therapeutic education of the diabetic patient].

Therapeutic education is a patient centred approach focused on patients' needs, values and strategies. It allows not only to increase patients' knowledge and skills on the disease, but also on their treatments. It brings a better quality of life, an increased therapeutic compliance, and decreases complications. The most difficult part of therapeutic education occurs when patients must change their behaviour. Motivational interviewing techniques are of great support and allow to prepare and support patients in "step by step" progressive changes. It is essential to work on resistance to change. The ambivalence in the choice of a new lifestyle must be measured, discussed and negotiate. Patients become partners and health care providers become coaches. To negotiate objectives must allow patients to choose their own strategies which should cost them minimum psychological efforts and bring them maximum benefits. The efficacy of therapeutic education has not to be proved any more: 80% less of amputations at 10 years in diabetic patients, 50% of stable body weight after weight loss at 5 years, etc. In conclusion, therapeutic education is part of a humanist medicine centred on patients which allow them to take care of their own treatment, in order to improve their quality of life, therapeutic compliance and potential complications. The health care providers teach, train, negotiate, motivate and accompany their patients in the long-term follow-up of their diseases.

Diabetes Complications↗

PubMedDate not supplied

Glucose disposal in obese non-diabetic and diabetic type II patients. A study by indirect calorimetry and euglycemic insulin clamp.

Insulin resistance is a characteristic finding in obesity and in non insulin dependent (Type II) diabetes mellitus. However, the interaction between diabetes and obesity has been poorly characterized and the metabolic disturbances contributing to the defect in insulin-mediated glucose uptake have not been defined. To examine these questions euglycemic and hyperinsulinemic clamp studies (40 mU/m2/min) were performed in 10 control non-obese subjects, 10 non diabetic obese subjects, 8 normal weight Type II diabetics, and 12 obese Type II diabetics. During the insulin clamp study total body glucose uptake in the obese non diabetics (157 +/- 18 mg/m2.min, p less than 0.01), the normal weight diabetics (159 +/- 21, p less than 0.01) and the obese diabetics (125 +/- 11, p less than 0.001) was significantly reduced compared to the non-obese non diabetic control group (249 +/- 22 mg/m2.min). The impairment in total body glucose uptake was the result mainly of a defect in non-oxidative glucose disposal. Indeed non-oxidative glucose disposal was blunted by 50% in the obese groups (p less than 0.01), somewhat less significantly in the non-obese diabetic group (p less than 0.05) but more when obesity and diabetes mellitus were combined (p less than 0.001). Total glucose oxidation was significantly diminished (p less than 0.01) in both diabetic groups but not in the obese non diabetic group when compared to lean control. A significant inverse correlation between the fasting free fatty acids levels and total glucose uptake (r = -0.453, p less than 0.001) and total glucose oxidation (r = -0.446, p less than 0.001) during the clamp was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Oxidative and nonoxidative glucose metabolism following graded doses of oral glucose in man.

The oxidative and nonoxidative glucose metabolism represent the two major mechanisms of the utilization of a glucose load. Eight normal subjects were administered oral loads of 50, 100 and 150 g glucose and gas exchange measurements were performed for eight hours by means of computerized continuous indirect calorimetry. The glycemic peaks were almost identical with all three doses with a rise to between 141 and 147 mg/dl at 60 min. The fall back to basal level was reached later with the high than with the low glucose doses. The glucose oxidation rate rose to values between 223 and 253 mg/min after the three glucose doses, but while falling immediately after the peak at 120 min following the 50 g load, the glucose oxidation rate remained at its maximum rate until 210 min for the 100 g glucose load and plateaued up to 270 min for the 150 g glucose dose. The oxidation rates then fell gradually to reach basal levels at 270, 330 and 420 min according to the increasing size of the load. Altogether 55 +/- 3 g glucose were oxidized during the 8 hours following the 50 g glucose load, 75 +/- 3 g after the 100 g load and 80 +/- 5 g after the 150 g load. The nonoxidative glucose disposal, which corresponds essentially to glucose storage, varied according to the size of the glucose load, with uptakes of 20 +/- 1, 60 +/- 1 and 110 +/- 1 g glucose 180 min after the 50, 100 and 150 g glucose loads respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMedDate not supplied

Evolution from obesity to diabetes.

The relationship between obesity and Type 2 diabetes mellitus is so closely related that it is worth questioning the possibility of obesity being more than just one diabetes risk factor among others but a factor which participates causally to the development of Type 2 Diabetes on a genetic background. In this review, the evolution of normal glucose tolerance towards impaired glucose tolerance corresponds to the development of compensatory metabolic changes. These compensatory mechanisms are hyperinsulinaemia and postprandial hyperglycaemia which prevents a defect in glucose uptake and especially glucose storage. These compensatory responses are overcome with time and diabetes develops in spite of the hyperinsulinaemia and the hyperglycaemia. The capacity for glucose storage is decreased and cannot be overcome at this stage by increases of both glucose and insulinemic responses. Inhibition of glycogen synthase activity by an increased muscle glycogen concentration is probably more powerful than its stimulation by insulin and glucose and the capacity for glucose storage remains decreased. Finally with time insulin secretion gradually decreases as a consequence of chronic hyperglycaemia and results in full pancreatic decompensation. At this stage hepatic glucose production is increased. The most important factor in the evolution from obesity to diabetes reside in the permanence of the increase in lipid oxidation and mainly in the duration of obesity. An important consequence of permanently high lipid oxidation is the chronic resistance to glucose uptake, initially compensated for by increased plasma insulin and glucose concentrations. A vicious circle starts after insulin resistance to glucose uptake appears, followed by hyperglycaemia blocking the glucose storage system and by the lack of storing capacity leading to a rise in glycaemia. In conclusion, all these metabolic phenomena are appearing in a sequential way, progressively adapting to the deteriorating situation, through the stages of normal glucose tolerance, impaired glucose tolerance, hyperinsulinaemic and finally hypoinsulinemic diabetes.

Blood Glucose↗