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Animal models of type 2 diabetes with reduced pancreatic beta-cell mass
No full textType 2 diabetes is increasingly viewed as a disease of insulin deficiency due not only to intrinsic pancreatic beta-cell dysfunction but also to reduction of beta-cell mass. It is likely that, in diabetes-prone subjects, the regulated beta-cell turnover that adapts cell mass to body's insulin requirements is impaired, presumably on a genetic basis. We still have a limited knowledge of how and when this derangement occurs and what might be the most effective therapeutic strategy to preserve beta-cell mass. The animal models of type 2 diabetes with reduced beta-cell mass described in this review can be extremely helpful (a) to have insight into the mechanisms underlying the defective growth or accelerated loss of beta-cells leading to the beta-cell mass reduction; (b) to investigate in prospective studies the mechanisms of compensatory adaptation and subsequent failure of a reduced beta-cell mass. Furthermore, these models are of invaluable importance to test the effectiveness of potential therapeutic agents that either stimulate beta-cell growth or inhibit beta-cell death
NICOTINAMIDE AND STREPTOZOTOCIN DIABETES IN RAT - FACTORS INFLUENCING EFFECTIVENESS OF PROTECTION
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Effects of a tryptophan load on brain levels of serotonin in normal and diabetic rats
No full textThe changes of brain tryptophan and 5-HT levels have been explored in the diabetic rat during the first hour after an intraperitoneal load of tryptophan. The obtained data confirm that diabetes decreases the basal levels of tryptophan but not those of 5-HT. Also, it has been shown that diabetes remarkably depresses the rate of the aminoacid accumulation and almost completely inhibits the rise of 5-HT after the tryptophan load
[Biochemical aspects of hormone-dependent muscles]. FT Aspetti biochimici di muscoli ormono-dipendenti
No full textDifferent sensitivity of muscle fibres to hormones might be an important factor in regulating differing properties of individual muscles, in addition to the well known neural effects on muscle fibres. The peculiar sensitivity of rat perineal muscles to androgens is a striking example, whose relevance to function is self explanatory in muscles connected with the sexual apparatus. Besides these qualitative differences, quantitative differences too can be observed when the responses of different muscles to hormones active on glycogen are compared. Data concerning the effects of androgens, insulin and hydrocortisone on perineal and skeletal muscles (soleus, gastrocnemius, extensor digitorum longus, quadricipes, obliquus externus abdominis and diaphragm) support this statement. However, the physiological meanings of these differences remain obscure
Calorie restriction counteracts the impairment of adipocyte insulin-stimulated lipogenesis in aging rats, but not that induced by dexamethasone treatment.
Full text linkIn order to detect metabolic derangements that could be implicated in the pathogenesis of age-related insulin resistance, insulin-stimulated lipogenesis was investigated in isolated adipocytes from 24-month-old Sprague-Dawley rats, and the protective influence of caloric restriction was assessed. For comparison, the effects of glucocorticoid administration, used as a pharmacological tool to alter insulin sensitivity, were also studied. Caloric restriction consisted in a 40% reduction of the daily food intake of controls starting at 3 months of age. Dexamethasone (0.13 mg/kg/day) was administered for 14 days prior to sacrifice to both ad libitum-fed and dietary-restricted aging rats. Three-month-old animals, treated or untreated with dexamethasone, served as young controls. The results showed a significant age-related decrease of insulin-stimulated lipogenesis, which was fully prevented by a lifelong regimen of dietary restriction. Dexamethasone treatment markedly reduced insulin-stimulated lipogenesis in adipocytes isolated from all groups of rats, including those submitted to calorie restriction. In conclusion, our data indicate that the mechanism by which aging alters adipose tissue insulin-induced lipogenesis is reversed by dietary intervention and appears to be different from that triggered by dexamethasone. This particular defect might contribute to an imbalance of fat distribution among tissues that could induce or aggravate peripheral insulin resistance in old age
FUNCTIONAL MODIFICATIONS OF ENDOCRINE PANCREAS AFTER INTERNAL BILIARY FISTULA (EXPERIMENTAL RESEARCH)
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