Background: Microsomal stearoyl-CoA desaturase1 (SCD1) is the rate limiting enzyme involved in the biosynthesis of monounsaturated fatty acids (MUFAs); palmitoleic (16:1) and oleic (18:1) acid from their respective substrates palmitic (16:0) and stearic (18:0) acids. The ratio of 18:1 to 18:0 has been implicated in the regulation membrane fluidity and function. SCD1 is abundantly expressed in obese humans as well as rodent models. However, no studies have correlated the fatty acid desaturation index (16:1/16:0 and 18:1/18:0), an indicator of SCD1 activity with the markers of obesity in terms of body mass index (BMI) and adiposity index (AI). Therefore, here, we attempted to relate the fatty acid desaturation index with BMI and AI in Wistar NIN-obese mutant rat strains namely, WNIN/Ob and WNIN/GR-Ob (with impaired glucose tolerance).

Metabolic experiments in rats were undertaken to relate excretory pattern of iodine and thiocyanate, with thyroid weight and the circulating levels of thyroxine, in response to moderate and high intake of iodine and under conditions of goitrogen induced altered thyroid status. On a moderate intake of iodine (by depriving diet of KI) 25 mg of thiocyanate or substitution of 1/3rd proportion of casein based diet with dry cabbage, could significantly reduce plasma thyroxine level by 60 days. Neither body weight nor the weights of liver, kidney, heart or spleen were affected due to exposure to goitrogens. A significant increase in thyroid weight as well as higher excretion of iodine and thiocyanate were evident in goitrogen-fed rats. Presence of high amounts of KI, to a certain extent, offered protection from adverse effects of the goitrogens. Semi quantitative assessment of thyroid, indicated hypofunctioning of thyroid with follicular hyperplasia in thiocyanate fed rats. These alterations were of moderate degree in response to cabbage feeding. These results emphasize that, moderate intake of iodine, adequate to meet iodine requirement, may not ensure normal functioning of thyroid in the presence of goitrogens.

The influence of nutritional inadequacy during the active growth phase of the developing brain, coinciding with myelinogenesis, was examined in rat pups. Developmental profiles of enzyme activities involved in biosynthesis of myelin membrane lipids, and those of associated pathways which generate precursor compounds for such biosynthetic reactions, were followed as functions of age in major anatomical regions of the brain. It was observed that while galactosyltransferase and choline phosphotransferase activities were significantly diminished, the microsomal cytochrome reductases, which contribute to the process of fatty acid elongation and desaturation, were also lowered. An attempt at adaptative increase of enzyme activity, in response to the stress, was apparent in the case of glycerol-3-phosphate dehydrogenase, which could possibly explain, in part, the lower susceptibility of phospholipid biosynthesis to impairments induced by nutritional insufficiency.

Food restriction was found to impair the incorporation of [1-14C]palmitate into myelin membrane lipids of developing rat brain. An attempt was made to determine whether this phenomenon is due to differences in the rate of utilization of the labelled precursor or to its enhanced degradation via beta-oxidative pathways. Undernutrition in pups was imposed by food restriction during gestation and lactation. beta-Oxidation by brain region homogenates using [1-14C]palmitate was monitored at days 7, 14 and 21 of postnatal age. There was a significant increase in beta-oxidation in the brain regions of undernourished pups, with the cerebrum and cerebellum being more affected than the brain stem. Because developing brain possesses the enzymic potential to utilize ketone bodies, the data may indicate increased usage of palmitate as an energy source in the developing brain of undernourished animals.