A new species of the neotropical catfish genus Trichomycterus (Siluriformes : Trichomycteridae) representing a new body shape for the family

Trichomycterus crassicaudatus is described as a new species from the Rio Iguacu basin in southern Brazil. The new species has an exceptionally deep posterior region of the body (caudal peduncle depth 22.8-25.4% SL), resulting in an overall shape which distinguishes it at once from all other members of the Trichomycteridae. The caudal fin of the species is broad-based and forked, a shape also distinguishing it from all other species in the family. A number of autapomorphic modifications of T. crassicaudatus are associated with the deepening of the caudal region, including an elongation of the hemal and neural spines of the vertebrae at the middle of the caudal peduncle. Phylogenetic relationships of the new species are yet unresolved, but it shares a similar color pattern and a thickening of caudal-fin procurrent rays with T. stawiarski, a poorly-known species also from the Rio Iguacu basin. Coloration and body shape also include similarities with T. lewi from Venezuela.

Changes in food intake, metabolic parameters and insulin resistance are induced by an isoenergetic, medium-chain fatty acid diet and are associated with modifications in insulin signalling in isolated rat pancreatic islets

LLong-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 (AKT1) 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.