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Biomedical subjects

E Kühn

Publications and source records attributed to E Kühn.

At least 19 recordsLinked to original sources
PubMed1998

Reproductive performance of rats treated with defatted jojoba meal or simmondsin before or during gestation.

The effects on food intake, growth and reproductive performance parameters of defatted jojoba meal and pure simmondsin, an extract from jojoba meal, were compared in female Wistar rats. Rats fed 0.15% simmondsin or 3% defatted jojoba meal (equivalent to 0.15% simmondsin) for 8 weeks before conception showed a similar reduction in food intake (about 20%) and a similar growth retardation compared with controls. Both treatments induced a reduction in the number of corpora lutea on gestation day 16: this effect could be ascribed to the lower food intake before conception because it was also observed in rats pair-fed to the treated ones. Rats given feed containing 0.15% simmondsin or 3% defatted jojoba meal during days 1-16 of gestation showed a similar reduction in food intake relative to controls. Foetal and placental weights were reduced, relative to controls, to a similar extent in both groups, and the reductions were slightly greater than in the corresponding pair-fed groups. We conclude that the effects on food intake, growth and reproductive performance that were seen after feeding rats defatted jojoba meal were due to the simmondsin content of the meal. The simmondsin induced reduction in food intake and probably also a relative protein shortage.

Acetonitriles↗
PubMed1998

Comparison of the effects of simmondsin and cholecystokinin on metabolism, brown adipose tissue and the pancreas in food-restricted rats.

In this study, we investigated the analogies between the physiological effects of simmondsin, a satiety-inducing glycoside extracted from jojoba seeds, and the gastro-intestinal satiation peptide, cholecystokinin. The effects of intraperitoneal injection of the biological active CCK-octapeptide on the pancreas, interscapular brown adipose tissue, growth performance and energy metabolism in normal-fed, severely food intake-restricted (50 % of normal food intake) or moderately food intake-restricted (65 % of normal food intake) growing rats were compared to the effects of 0.25 % simmondsin mixed in the food, inducing moderate food intake reduction (65 % of normal) in rats. Cholecystokinin induced pancreatic hypertrophy. In normal fed rats, cholecystokinin had no effect on brown adipose tissue or growth, while, in severely food intake-restricted rats, it caused brown adipose tissue hypertrophy and reduced growth. In moderately food intake-restricted rats, both cholecystokinin and simmondsin induced pancreatic hypertrophy, increased brown adipose weight and metabolism and caused a slight decrease in growth. We conclude that cholecystokinin may decrease growth performance in fast growing severely food intake-restricted rats by stimulating brown adipose tissue metabolism, probably because of protein shortage induced by pancreatic hyperstimulation. Simmondsin has similar effects. These results support the hypothesis that endogenous cholecystokinin is involved in the effects of simmondsin in rats.

Acetonitriles↗
PubMed1995

Devazepide reverses the anorexic effect of simmondsin in the rat.

Simmondsin, a glycoside extracted from jojoba meal (Simmondsia chinensis), causes a reduction in food intake after oral administration. To investigate the mechanism by which simmondsin reduces food intake, fasted and free-feeding rats were given simmondsin-supplemented food and simultaneously injected with devazepide, a specific antagonist of peripheral-type cholecystokinin receptors (CCKA receptors). In free-feeding rats, supplementation of food with 0.5% simmondsin caused a reduction in food intake of +/- 40% in the period of 4 h following food presentation. Intraperitoneal injection of 100 micrograms devazepide/kg body weight prevented this effect. In rats fasted for 20 h, the food intake in the 30 min after presentation of food supplemented with 0.15% or 0.50% simmondsin was reduced in a dose-related manner; this was also inhibited by simultaneous application of devazepide. It is suggested that peripheral CCKA receptors are involved in the effect of simmondsin on food intake. However, a direct effect of simmondsin on CCKA receptors has been excluded, since simmondsin was unable to cause contraction of the guinea-pig gallbladder in vitro.

Acetonitriles↗
PubMed1990

Effects of dietary T3 on growth parameters and hormone levels in normal and sex-linked dwarf chickens.

Tri-iodothyronine (T3) has been administered in the diet, from day of hatch until 8 weeks of age, to sex-linked dwarf and normal chicks of both sexes from a brown-egg slow-growing strain. Feed was supplemented with either 0.1 ppm or 0.5 ppm T3. A significant genotype by treatment interaction was observed on body weight: the effect of T3 in males was significantly positive for dwarfs and null for normals, the effect in females was null for dwarfs and significantly negative for normals. Feed efficiency was rather decreased by the treatment in both genotypes. Abdominal fatness was decreased in a dose-dependent manner in both genotypes, while rectal temperature was raised in dwarf chicks only. Plasma T3 was raised to normal levels in dwarfs receiving 0.1 ppm exogenous T3, while the 0.5 ppm dose yielded hyperthyroid levels. Plasma GH levels were decreased in a dose-dependent manner by the T3 treatment, the effect being larger in dwarfs. Surprisingly, plasma IGF-I was unchanged in spite of the GH decrease, whatever the genotype or the sex. It was concluded that exogenous T3 alone can have a stimulatory effect on growth in dwarfs but can not fully restore a normal growth rate. Both T3 and IGF-I are important for a normal growth and the relationship between T3 and IGF-I production should be further investigated in order to better understand the physiological modifications due to the sex-linked dwarf gene.

Abdomen↗