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Biomedical subjects

K D Hepp

Publications and source records attributed to K D Hepp.

At least 37 records · Page 2Linked to original sources
PubMed1988

[The early breakfast--an unknown pitfall in the treatment of type-I diabetes mellitus].

In 15 type I diabetics the mean postprandial rise in blood glucose levels, 90 min after breakfast at about 8 a.m. (the customary time for this meal in hospitals), was 62.2 +/- 34.3 mg/dl, but 90 min after a breakfast which had been put forward by about 1 1/2 hours it was only 2.6 +/- 18.6 mg/dl (P less than 0.001). Seven patients developed hypoglycaemia after the early breakfast, none after the late one. This finding suggests that, to avoid hypoglycaemia after an early breakfast, an additional small meal should be given at about 8:30 a.m. or the insulin content of the morning injection should be changed. The clear connection between the time of the morning insulin injection and the insulin action during the morning explains why, in uninstructed patients who--under their usual daily conditions of starting school or work--are forced to inject insulin early or to eat early, a state of hypoglycaemia may occur.

Adult↗
PubMed1986

[Comparison of the effects of protamine-bound NPH porcine insulin and NPH human insulin in type 1 and 2 diabetes].

Porcine and semisynthetic human insulin preparations (Nordisk) having the same content of regular insulin, same galenic characteristics and same degree of purity, were tested in type I, type IIa and type IIb diabetics. There was no difference as to the duration of action. This is contrary to some earlier reports stating that protamine-bound biosynthetic human insulin has a shorter duration of action than porcine preparations. The onset of the hypoglycaemic action in type IIa diabetics is significantly more rapid with isophane human insulin than with isophane pork insulin. The use of an insulin pump prior to testing the duration of action of intermediate insulin preparations appears to be superior to other methods.

Aged↗
PubMed1982

Glucose control in mobile type 1 (insulin-dependent) diabetic patients by means of a semi-automatic feedback controlled insulin infusion system.

A portable insulin dosing device (Siemens) was used together with a programmable pocket calculator and a glucose analyzer for short-term adaptation of continuous intravenous insulin infusion to blood glucose alterations. A special algorithm was developed which utilizes a given blood glucose value and the glucose rate of change obtained from two to four consecutive samples as input variables. In contrast to current techniques of feedback-regulation, which require continuous glucose monitoring, intermittent blood sampling allows greater mobility of patients. With the semi-automatic feedback system, euglycaemic control was obtained for 12-h periods in ten Type 1 (insulin-dependent) diabetic patients (maximum value 9.50 mmol/l, minimum value 2.83 mmol/l). Severe hypoglycaemia occurred in no case and additional control by glucose infusion appeared to be unnecessary. Light exercise after termination of insulin dose for standard meals led to glycaemic excursions with a rapid decrease (mean 1.08 +/- 0.09 mmol/l), followed by a rebound (0.59 +/- 0.07 mmol/l) in each patient. The amplitude of these excursions decreased with increasing distance from the peak of the meal dose. Comparison of feedback-control alone with feedback by glucose plus preprogrammed dose (4 U/h) at the onset of the test meal revealed lower post-prandial glucose levels (post-prandial maximum +/- SEM: 6.49 +/- 0.18 versus 7.71 +/- 0.79 mmol/l) and a lower infusion rate of insulin for the combined regimen (mean post-prandial maximum +/- SEM: 8.4 +/- 1.2 versus 12.0 +/- 0 IU/h). The system is useful for programming of portable infusion devices and studies based on euglycaemic control in unrestrained patients.

Adult↗
PubMed1982

Increased dose-response relationship of liver plasma membrane adenylate cyclase to glucagon stimulation in diabetic rats. A possible role of the guanyl nucleotide-binding regulatory protein.

In view of controversial findings regarding the mechanism for the increased intracellular hepatic cyclic 3':5' adenosine monophosphate levels in diabetic rats, we studied the dose-response relationship of the adenylate cyclase to glucagon stimulation in severely diabetic and in diabetic, insulin-treated rats. An enhanced response to glucagon and an additional augmenting effect of guanosine triphosphate on hormonal stimulation of the adenylate cyclase activity were found in diabetes which were reversible with insulin treatment. The results suggest a role of the regulatory guanyl nucleotide-binding protein in diabetes leading to an increased dose response relationship of the hepatic adenylate cyclase system to glucagon.

Adenylyl Cyclases↗
PubMed1980

Insulin binding and insulin action in rat fat cells after adrenalectomy.

Insulin binding and the effect of insulin on the transport of 3-O-methylglucose, lipogenesis from glucose, glucose oxidation and lipolysis was studied in fat cells of adrenalectomised rats and of a control group of sham-operated rats. The serum insulin level of the adrenalectomised rats (0.7 ng/ml) was lower than that of the controls (1.6 ng/ml). In adrenalectomised rats as compared to sham-operated rats the insulin concentrations causing half-maximal effect were reduced by 50% in lipogenesis and antilipolysis and by 30% in glucose transport. The increase in sensitivity to submaximal insulin concentrations was not observed in glucose oxidation. The maximal responsiveness was unchanged in all test systems. The increase in sensitivity in three of the four studied insulin effects may be related to the 37% increase in the binding capacity of fat cells from adrenalectomised compared with sham-operated rats. The unchanged sensitivity with respect to glucose oxidation indicates possible post-receptor modulation. When adrenalectomised rats were substituted with either insulin or cortisol serum insulin levels were elevated above normal; however, the changes in the receptor were prevented in the cortisol supplemented rats and only partially in the insulin supplemented rats. The observation suggests, that the insulin receptor is regulated not only by the serum insulin level but also by cortisol.

Adipose Tissue↗