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Long-chain fatty acids are capable of inducing alterations in the homoeostasis of glucose-stimulated insulin secretion (GSIS), but the effect of medium-chain fatty acids (MCFA) is poorly elucidated. In the present study, we fed a normoenergetic MCFA diet to male rats from the age of 1 month to the age of 4 months in order to analyse the effect of MCFA on body growth, insulin sensitivity and GSIS. The 45 % MCFA substitution of whole fatty acids in the normoenergetic diet impaired whole body growth and resulted in increased body adiposity and hyperinsulinaemia, and reduced insulin-mediated glucose uptake in skeletal muscle. In addition, the isolated pancreatic islets from the MCFA-fed rats showed impaired GSIS and reduced protein kinase Ba (AKT 1 ) protein expression and extracellular signal-related kinase isoforms 1 and 2 (ERK 1/2 ) phosphorylation, which were accompanied by increased cellular death. Furthermore, there was a mildly increased cholinergic sensitivity to GSIS. We discuss these findings in further detail, and advocate that they might have a role in the mechanistic pathway leading to the compensatory hyperinsulinaemic status found in this animal model.

An investigative study was carried out for 2 years involving 124 randomly selected early postmenopausal women with spine bone mineral density (BMD) below the mean value of a normal premenopausal subject. After random division into three groups, the first 42 patients were treated with transcutaneous 17-beta-estradiol (50 micrograms daily), the second 42 were treated with cyclical intravenous clodronate (200 mg/month iv infusion), and the third group of 40 (controls) was left untreated. After 2 years, the total drop in BMD within the control group was more than 7% as opposed to the values of -0.14% +/- 0.93 in the estradiol group and 0.67% +/- 0.84 in the clodronate group. A change in BMD of < 1% was considered satisfactory, and this result was obtained in 32% of the controls, in 79% of the estradiol group where the percentage change in BMD moderately correlated with serum estradiol levels (r = 0.399), and in 90% of the clodronate-treated patients, in whom the percentage change in BMD inversely correlated with basal values of markers of bone turnover. Both estrogen and clodronate prevent postmenopausal bone loss. The response to transcutaneous hormone replacement therapy may be influenced by transcutaneous absorption and by a lower sensitivity to estrogen. Response to cyclical clodronate seems to be influenced by the rate of bone turnover. An interdosage interval ranging from 2-4 weeks appears suitable for most patients.

The effects of protein malnutrition, both in utero and prior to weaning, on formation of the first mandibular molars were evaluated by phase-contrast and electron microscopy in rats. The nourished group (GI) received a diet that included 20% casein, while the malnourished group (GII) received 5% casein. The first mandibular molars from GII exhibited low density of cells and odontoblasts, which lacked regular organization compared with molars from GI. In addition, a difference in collagen type was observed between the groups, with a prevalence of Type III collagen fibers detected in the dentin, periodontal ligament, and alveolar bone of GII, and a prevalence of Type I collagen fibers in GI. Finally, examination of surface area in molar sagittal sections indicated 30% less dentin in GII, compared with GI. Our results suggest that structural and ultra-structural features of the dentin-pulp complex and periodontal components of rat molars are affected by protein deficiency.

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