[Need for control in the workplace and motivation for alcohol consumption: a written survey in 3 public civil service agencies]. / Kontrollambitionen am Arbeitsplatz und die Motivation zum Alkoholkonsum: Eine schriftliche Befragung in drei öffentlichen Verwaltungen.

The links between the need for control (inability to withdraw from work obligations and work commitment) at the workplace and the motivation to consume alcohol is investigated on the basis of 427 male employees in three public administrations or spatially and organizationally homogenous parts of these administrations. By analogy with the work of McClelland and with reference to the concept of the need for control it is conjectured that a link exists between the need for control and the motivation to consume alcohol as a means of coping with stress. Using a linear-additive regression model it becomes evident that the inability to withdraw from work obligations though not the work commitment have an effect on the consumption motive. This effect is not eliminated by the tendency for social desirability and the salary grouping, which are included in the regression model as predictors. In summary, the data proves a link between the inability to withdraw from work obligations on the one side and the consumption of alcohol as a means of coping with stress on the other.

Inhibitors of the rate of carbohydrate and lipid absorption by the intestine.

The rate of energy storage in adipose tissues is, at least in part, dependent on the concentration of nutrients and hormones in the blood. A delayed absorption of ingesta from the intestine should cause lower concentrations of fat, glucose and insulin and, thus, reduce the triglyceride storage rate. Non-selective agents retard the absorption irrespective of composition of food. Inhibitors of intestinal alpha-glucosidases delay the degradation of complex carbohydrates to absorbable monosaccharides and thus decrease the rate of their absorption. Inhibitors of pancreatic lipase interfere with the degradation of dietary triglycerides and decrease the postprandial triglyceride increment in blood and tissues. Recently a compound was found which inhibits the absorption of carbohydrates as well as triglycerides.

Reduction of carbohydrate-induced hypertriglyceridemia in (fa,fa) "Zucker" rats by the alpha-glucosidase inhibitor acarbose (BAY g 5421).

Inhibition of carbohydrate digestion by the alpha-glucosidase inhibitor acarbose (BAY g 5421)reduces carbohydrate-induced postprandial blood glucose increase and insulin secretion. As a consequence, in feeding experiments sucrose-induced hyperinsulinemia and hypertriglyceridemia in genetically obese (fa,fa) "Zucker" rats were dose-dependently reduced by addition of acarbose to the diet (15-80 mg/100 g feed). The body weight gain was dose-dependently reduced. In short-term experiments with a fat-free diet acarbose not only prevented serum triglyceride and free fatty acid increase in spite of lowered insulin concentrations but also decreased their concentrations below the values obtained on standard feed. Under these conditions there were no significant effects on body weight. Hypertriglyceridemia induced by i.v. injection of the lipoprotein lipase inhibitor Triton WR 1339 was reduced without affecting body weight in "Zucker" rats after 3 days on a fat-free diet supplemented with acarbose. The triglyceride increase was even lower than in animals kept on standard feed. The data demonstrate that acarbose reduces sucrose-induced hypertriglyceridemia in (fa,fa) "Zucker" rats by diminishing VLDL production and/or secretion rather than by increasing VLDL removal from the blood.

Inhibition of disaccharide digestion in rat intestine by the alpha-glucosidase inhibitor acarbose (BAY g 5421).

Administration of the alpha-glucosidase inhibitor, acarbose (BAY g 5421), to rats together with a sucrose load results in a marked retardation of sucrose digestion. The carbohydrate content of the small intestine is dose dependently increased; the time needed for the absorption is doubled. In the large intestine significant amounts of carbohydrate can be found only after administration of high doses of acarbose (2-4 mg/kg p.o.). In oral sucrose and maltose loading tests the blood glucose increase is dose dependently reduced by acarbose (ED50, 1 or 12 mg/kg, respectively). In perfused jejunal loops of rats, acarbose inhibits the absorption of sucrose (4 g/l) and maltose (1 and 2 g/l), the IC50 values being 3.2, 36, and 57 micrograms/ml, respectively. The data indicate that acarbose effectively inhibits sucrose digestion. It is 10-20 times less effective with maltose as a substrate. Slight malabsorption is induced by acarbose only in doses higher than the ED50.

[3-Amino-2H-1,2,4-benzothiadiazine-1,1-dioxides with antihypertensive and possibly diabetogenic activity (author's transl)]. / 3-Amino-2H-1,2,4-benzothiadiazin-1,1-dioxide mit antihypertensiver und potentieller diabetogener Wirkung.

By reaction of dialkylaminoalkylamines or omega-amino-alkylethers with 2H-1,2,4-benzothiadiazine-1,1-dioxides bearing a group in the 3-position labile towards nucleophilic substitution (Cl, CH3S, CH3CO2), the corresponding 3-substituted amino-2H-1,2,4-benzothiadiazine-1,1-dioxides are obtained. A series of these compounds exerts an antihypertensive effect in the renally hypertonic rat after oral administration and in the "two-kidney hypertensive dog" after parenteral administration. Two compounds (1 and 4) were studied thoroughly in comparison to diazoxide (16) and the known piperazino compound (17). At 10 mg/kg in the rat, diazoxide causes a marked reduction of water and electrolyte excretion but at this dosage 1 and 4 are neither diuretic nor antidiuretic. In the hyperglycaemia test on normal rats at a dosage 30--100 times that required for an antihypertensive effect, 1 and 4 show after 300 mg/kg no hyperglycaemic effect and after 1000 mg/kg p.o. a very weak one. 17 has a weak hyperglycaemic effect at 300 mg/kg diazoxide a strong one. However, intensive glucose loading studies on diabetic rats (reduced glucose-tolerance) and on metabolically healthy rats with glucose loading showed that compounds 1 and 4 as well as the piperazine derivative 17 inhibit insulin release, albeit in higher doses than does diazoxide. In animals with insulin resistance a diabetic metabolic condition occurs with high blood-sugar levels. Owing to this possible diabetogenic activity, testing and application of 1, 4 and the known 7-chloro-3-(4-methyl-1-piperazinyl)-2H-1,2,4-benzothiadiazine-1,1-dioxide for blood-sugar lowering activity to human volunteers is not considered appropriate.

Inhibition of sucrase by tris in rat and man, demonstrated by oral loading tests with sucrose.

In the course of work concerned with the inhibition of small intestinal carbohydrate digesting enzymes, experiments were performed on rats and two healthy volunteers using tris as a sucrase inhibitor. The following results were obtained: (1) Tris does not lower the blood glucose in fasting rats after oral or subcutaneous doses up to 500 mg/kg, when administered as neutral solution (pH 7.0). (2) Tris reduces reduces the glycemia in rats and human subjects after a sucrose load. In addition, the insulinemia caused by administration of sucrose is reduced in man. This smoothing effect on both curves is dose-dependent. A delay of gastric emptying by tris could be excluded. (3) After a glucose or matose load in rats, tris has no effect on the blood sugar curve. (4) The marked smoothing effect of tris is after sucrose loading is probably caused by its well-known in vitro inhibitory effect on intestinal sucrase activity of pigs and humans.