Maternal conjugated linoleic acid supplementation reverses high-fat diet-induced skeletal muscle atrophy and inflammation in adult male rat offspring.

A high-saturated-fat diet (HFD) during pregnancy and lactation leads to metabolic disorders in offspring concomitant with increased adiposity and a proinflammatory phenotype in later life. During the fetal period, the impact of maternal diet on skeletal muscle development is poorly described, despite this tissue exerting a major influence on life-long metabolic health. This study investigated the effect of a maternal HFD on skeletal muscle anabolic, catabolic, and inflammatory signaling in adult rat offspring. Furthermore, the actions of maternal-supplemented conjugated linoleic acid (CLA) on these measures of muscle phenotype were investigated. A purified control diet (CD; 10% kcal fat), a CD supplemented with CLA (CLA; 10% kcal fat, 1% total fat as CLA), a high-fat (HFD; 45% kcal fat from lard), or a HFD supplemented with CLA (HFCLA; 45% kcal fat from lard, 1% total fat as CLA) was fed ad libitum to female Sprague-Dawley rats for 10 days before mating and throughout gestation and lactation. Male offspring received a standard chow diet from weaning, and the gastrocnemius was collected for analysis at day 150. Offspring from HF and HFCLA mothers displayed lower muscular protein content accompanied by elevated monocyte chemotactic protein-1, IL-6, and IL-1ß concentrations. Phosphorylation of NF-κBp65 (Ser(536)) and expression of the catabolic E3 ligase muscle ring finger 1 (MuRF1) were increased in HF offspring, an effect reversed by maternal CLA supplementation. The present study demonstrates the importance of early life interventions to ameliorate the negative effects of poor maternal diet on offspring skeletal muscle development.

Odontoblast transport of sulphate--the in vitro influence of fluoride.

The present study reports the development of a culture system for the analysis of 35S-sulphate release from odontoblasts in vitro. Pulpless longitudinally split rat incisors were cultured in supplemented minimum essential medium (alphaMEM) with 20 microCi 35S-sulphate per ml, 20 microCi 3H-mannitol per ml for 1h. Teeth were then transferred to fresh unlabelled media and aliquots of media were removed and the level of 35S-sulphate 3H-mannitol determined. Results indicated a two phase release of 35S-sulphate into the media, and comparison with pulp tissue indicated a specific release pattern. Transport of sulphate is essential for correct synthesis and glycosylation of macromolecules such as proteoglycans (PG). Previous studies have shown that post-translational modifications of these proteins can be influenced by excess fluoride, resulting in decreased sulphation and elongation of glycosaminoglycan (GAG) chains. Therefore the influence of fluoride on sulphate transport, using the optimised culture system was also investigated. Inclusion of 6mM fluoride during pulse labelling caused a significant decrease of 35S-sulphate (P<0.0001) during the initial release phase. Inclusion of 3 and 6mM fluoride only in the post-labelling incubation media resulted in a significant decrease in the release of 35S-sulphate (P<0.0001), during the total time course. The influence of fluoride was not dose dependent. Inclusion of a specific chloride channel blocker SITS, into the culture system indicated that 35S-sulphate transport may in part be via this route. Fluoride would therefore appear to influence the transport of 35S-sulphate across the odontoblast membrane, potentially via a chloride channel.