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G Dietze

Publications and source records attributed to G Dietze.

At least 37 records · Page 2Linked to original sources
PubMed1990

[Essential hypertension and diabetes mellitus].

While the incidence of essential hypertension is not increased in type 1 diabetics, it is about three times as high in type 2 diabetics. Since in 50% of the cases, hypertension is present before the metabolic disorder becomes manifest, an association between the etiologies of the two disturbances was suspected as long as 65 years ago. A new understanding of the significance of insulin resistance and hyperinsulinemia suggests that the two conditions are part of a single metabolic disorder. This is supported by the fact that normal-weight hypertensives can also manifest insulin resistance, and they more often develop a type 2 diabetes mellitus. These facts urge us to re-think our therapeutic approach to hypertension, and to employ, as far as possible, only those substances that have no negative influence on the incidence of the metabolic disorder. With the introduction of ACE-inhibitors capable of improving insulin sensitivity, we now have, for the first time, the possibility of improving the prognosis of the metabolic syndrome. Moreover, their molecular mechanism of action provides initial clues as to the possible etiology of the syndrome.

Diabetes Mellitus, Type 1↗
PubMed1990

Effects of beta-blocking agents on insulin secretion and glucose disposal.

Non-selective and to a lesser extent selective beta-blockers are known to slightly deteriorate glucose metabolism. This may be of clinical relevance, since patients with essential hypertension suffer from reduced insulin-sensitivity and some studies showed an increased incidence of diabetes type II with beta-blocker-treated hypertensive patients. However, it is not clear whether this effect is due to hypertension per se or in addition by antihypertensive treatment. The possible mechanisms by which beta-blockers influence carbohydrate metabolism are discussed. Insulin secretion is inhibited by beta-blockers in vitro. However, no effect is seen in vivo in man. Hepatic glucose production in theory may be influenced, but no effect is demonstrable. Muscular glucose uptake could be reduced; some data exist showing reduced peripheral insulin sensitivity, although there are controversial results. In conclusion, a deterioration of carbohydrate metabolism by beta-blockers is established, the mechanism whereby remains obscure.

Adrenergic beta-Antagonists↗
PubMed1990

Clinical studies with CE-inhibitors in diabetes.

Early antihypertensive intervention in diabetes often means intervention in a cluster of cardiovascular risk factors including glucose intolerance per se, hyperlipidemia, obesity and hypertension, which are not just coexistent but may be causally linked together by the resistance of peripheral tissues to the action of insulin. Blood pressure lowering treatment should therefore be metabolically neutral in order to avoid aggravation of this risk factor syndrome. Clinical studies applying CE-inhibitors in type II diabetes are critically reviewed under this aspect. The majority of the available studies in type II diabetes report a reduction of insulin resistance and a marginal improvement of metabolic control. The order of magnitude in HbA1 reduction is nearly 10% of the glycosylated haemoglobin, reduction of fasting and postprandial blood glucose approximates 1 mmol/l. From a more extended view, considering essential hypertension as insulin resistant and thus possibly "prediabetic" state, this marginal metabolic effect gets further support from recent studies in essential hypertension consistently reporting an improvement of metabolic parameters of similar magnitude. This might become a central argument in the discussion about individualized and metabolically neutral antihypertensive treatment in essential hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Local generation of kinins in working skeletal muscle tissue in man.

The effect of standardized isometric forearm work on circulating and local kinin concentrations was investigated in 12 healthy volunteers using the forearm catheter technique. Radioimmunological kinin determination in arterial blood and in the venous effluent of forearm muscle tissue was performed using a modification of Shimamoto's technique of blood sampling and kinin extraction. Under basal conditions, there was no arterio-venous difference of kinins. Throughout the whole experiment, arterial--reflecting systemically circulating--kinins did not change. In muscle venous blood, immunoreactive kinins were not significantly elevated during work, whereas a marked increase was detected in the recovery period (5.0 +/- 0.6 vs. 10.2 +/- 2.0 pmol/l; p less than 0.01). The data demonstrate, that kinins are locally generated in calculated amounts (32.7 +/- 8.4 fmol/(100 g x min) that are known to be sufficient to induce local vasodilatory and metabolic effects at the site of muscle contraction, but below the threshold for systemic cardiovascular actions.

Adult↗
PubMed1989

[Artificial nutrition of diabetic patients].

For total parenteral nutrition in diabetes, the same relation between carbohydrates, fat and protein of 50, 30-35 and 15-20% of total calories as in regular oral feeding has to be taken. For carbohydrates, a 2:1:1 mixture of fructose, glucose and xylitol should be used, since this is to a lesser extent blood glucose level raising as glucose alone and the dose-dependent side effects of the sugar substitutes are negligible. If insulin is infused intravenously, it is important that the carbohydrates are given simultaneously, in order to prevent deleterious hypoglycemnia. Mixtures of MCT and LCT are to be preferred towards pure LCT-emulsions, since the faster elimination of MCT/LCT-solutions may be of clinical relevance in diabetics type II, who frequently have a disturbed lipid metabolism. For protein, the normal amino acid pattern can be used, special solutions are not necessary.

Diabetes Mellitus↗
PubMed1989

The kallikrein/kinin system in the pathogenesis of hypertension in diabetes mellitus.

Essential hypertension (EH) is frequently not only a coexistent, but a preexistent condition in type-II-diabetes mellitus (NIDDM). Possible reasons for this phenomenon include the presence of the insulin resistance/hyperinsulinaemia syndrome in EH, leading to sodium retention, stimulation of the sympathetic nervous system and impaired glucose tolerance. Another reason could be a defect in the kallikrein-kinin system (KKS) which is known to be involved in both the regulation of blood pressure and insulin sensitivity of peripheral tissues. The classical concept of the glandular KKS as being an endocrine system with circulating hormones causing increased renal and peripheral blood flow, hypotension and natriuresis has changed recently, since kallikrein-like activity or mRNA coding for tissue kallikreins were detected in various tissues including kidney, vascular wall and skeletal muscle. This led to the present view, that paracrine local actions of different tissue KKS on regional blood flow, local substrate metabolism and insulin action are probably more important than previously expected. A disorder in the activity of the renal KKS has been known to be present in both NIDDM and EH. Recent work yielded evidence, that skeletal muscle KKS is activated upon muscle work in metabolically healthy subjects, but not in NIDDM and not in the majority of patients with EH. This suppressed tissue KKS seems to be a common feature of EH and NIDDM and might be involved in the pathogenesis of insulin resistance, impaired glucose tolerance and hypertension.

Amino Acids↗
PubMed1988

[Improved insulin action by ACE inhibition in type-2 diabetics].

The effect of the angiotensin converting enzyme inhibitor captopril (25 mg by mouth) on glucose metabolism of skeletal muscle and the whole organism was studied in nine normotensive type II (non-insulin dependent) diabetics using a combination of euglycaemic-hyperinsulinaemic glucose-clamp and forearm catheter techniques. The administration of captopril resulted in a significant rise of both the whole-body glucose elimination and utilization rate in the forearm musculature. At the same time the arterial kinin level rose, while the concentrations of insulin, free fatty acids and gluconeogenesis precursors, as well as the number and activity of insulin receptors (measured in an erythrocyte-binding study) remained unchanged. The data support the view that, in type II diabetics, ACE inhibition raises the insulin-stimulated glucose uptake of the whole organism, predominantly due to an increased glucose uptake by the skeletal musculature. The demonstration of an increased kinin level points to this effect possibly being caused by the reduced breakdown of locally liberated kinins.

Axilla↗
PubMed1988

Inhibition of muscular ketone extraction by lipid infusion in man.

Using the forearm technique, muscular ketone body metabolism was investigated in 12 healthy volunteers during an i.v. infusion of lipid emulsions containing long chain triglycerides (LCT) or a mixture of medium- and long chain triglycerides (MCT/LCT). During the basal period, arterial concentrations and muscular extraction of beta-hydroxybutyrate and acetoacetate were linearly correlated as expected. This relationship was abolished during the infusion of both lipid emulsions. In addition, fractional extraction rates of ketone bodies were reduced. These changes were most probably mediated by elevated levels of free fatty acids and triglycerides as well.

3-Hydroxybutyric Acid↗
PubMed1988

Determination of absorbed dose within an A150 plastic phantom for a d(13.5 MeV) + Be neutron source.

In the collimated beam of a d(13.35 MeV) + Be neutron source the total absorbed dose within an A150 plastic phantom was determined using three independent methods: the twin-detector method, measurements with a tissue-equivalent calorimeter and a Monte Carlo calculation of the spectral neutron fluence within the phantom. The front of the cubic phantom was positioned at a distance of 800 mm from the neutron source. the absorbed dose data obtained by the three methods at phantom depths of 27 and 52 mm are consistent within their uncertainties. Between phantom depths of 10 and 60 mm a mean dose gradient of (1.61 +/- 0.02) Gy C-1 mm-1 has been derived.

Absorptiometry, Photon↗
PubMed1988

Role of angiotensin-converting enzyme inhibitors in early antihypertensive treatment in non-insulin dependent diabetes mellitus.

The effect of captopril monotherapy on blood pressure and metabolism was investigated in a placebo-controlled study in 30 non-insulin dependent (Type II) diabetic subjects during a 3-week observation period (run-in/drug; placebo/wash-out) on a metabolic ward. Captopril significantly reduced both systolic and diastolic blood pressure (154/90 +/- 5/2 vs. 144/86 +/- 4/3 mmHg) without major side effects. Mean run-in postprandial blood glucose concentrations were also reduced upon ACE-inhibition (9 a.m.: 12.7 +/- 0.4 vs. 11.1 +/- 0.4 mmol/l; 1 p.m.: 11.0 +/- 0.3 vs. 8.9 +/- 0.3 mmol/l; P less than 0.05), while blood kinin concentrations (40.0 +/- 2.5 pmol/l) were approximately doubled (108.8 +/- 23.5 pmol/l; P less than 0.05). Body mass index, fasting plasma insulin, serum electrolyte pattern, uric acid, white blood count, lipid profile as well as hepatic and renal function parameters remained unaltered throughout the observation period. The data are in line with recent experimental studies showing a beneficial metabolic effect of captopril in Type II diabetes. ACE inhibitors might therefore become first-line drugs in early antihypertensive intervention in Type II diabetic patients.

Aged↗
PubMed1988

[Changes in ultrasonic findings in the liver in relation to parenteral nutrition with long chain triglyceride and medium chain triglyceride/long chain triglyceride lipid solutions].

Fatty infiltration of the liver with cholestasis is one of the complications of total parenteral nutrition (TPN). The casualty has not yet been determined. It seems probable, however, that these alterations could be prevented when a mixture of medium- and long-chain triglycerides (MCT/LCT) is used as fat component of TPN instead of the application of long-chain emulsions (LCT) alone. To determine whether this could be demonstrated also morphologically in man, 14 patients needing TPN (25 kcal/kg BW x d, CH 45%, F 35%, P 20%) were examined with ultrasound in order to compare liver-size and grey-scale value before and after 7 days of TPN. Seven of the patients were randomly given as their fat-intake an MCT/LCT-emulsion, the other 7 LCT exclusively. There were no changes in liver size and grey-scale value in the MCT/LCT-group, whereas both parameters showed a significant rise in the patients with LCT (size: 10.4 +/- 1.4 to 11.5 +/- 1.4 cm; grey-scale value: 9.3 +/- 1.0 to 11.6 +/- 0.7). These data suggest that TPN, administered with a mixture of MCT/LCT emulsions as fat component, could reduce the risk of hepatic dysfunction such as cholestasis and fatty infiltration of the liver.

Fat Emulsions, Intravenous↗