エジプト紅海沿岸のマングローブ林の林分構造

Established mangrove forests along the coastal area of the Arabian Peninsula and African side of the Red Sea are uniquely different from mangrove forests in other parts of the world because of their low biodiversity and harsh habitat of arid and highly saline conditions. Therefore mangrove forests in this area appear in patchy and scattered patterns at mouths of wadi or in sheltered lagoons with rare and irregular flooding. Most of them are pure forests of Avicennia marina, occasionally mixed with Rhizophora mucronata in the southern part of the Red Sea. In this study, we analyze the forest structure of A. marina and discuss the regeneration strategy and the forest dynamics of this unique mangrove species. Three experimental plots of 1000 to 2000 trees/ha were selected from north to south along the Red Sea coast. The highest tree size (6.8m) suggested severe effects of the high salinity of the Red Sea (3.2 to 4.9%) on tree growth. Dense mantle vegetation had developed at the forest edge facing the open sea to protect the forest interior against strong waves and wind. Tree growth was also prevented by severe drought on the landside edge of the forest. All the forests had a dense seedling bank throughout the forest floor, with a very high rate of turnover and regeneration, which seldom occurred in other forests

Activation of peroxisome proliferator-activated receptor-alpha stimulates both differentiation and fatty acid oxidation in adipocytes[S]

Peroxisome proliferator-activated receptor-α (PPARα) is a dietary lipid sensor, whose activation results in hypolipidemic effects. In this study, we investigated whether PPARα activation affects energy metabolism in white adipose tissue (WAT). Activation of PPARα by its agonist (bezafibrate) markedly reduced adiposity in KK mice fed a high-fat diet. In 3T3-L1 adipocytes, addition of GW7647, a highly specific PPARα agonist, during adipocyte differentiation enhanced glycerol-3-phosphate dehydrogenase activity, insulin-stimulated glucose uptake, and adipogenic gene expression. However, triglyceride accumulation was not increased by PPARα activation. PPARα activation induced expression of target genes involved in FA oxidation and stimulated FA oxidation. In WAT of KK mice treated with bezafibrate, both adipogenic and FA oxidation-related genes were significantly upregulated. These changes in mRNA expression were not observed in PPARα-deficient mice. Bezafibrate treatment enhanced FA oxidation in isolated adipocytes, suppressing adipocyte hypertrophy. Chromatin immunoprecipitation (ChIP) assay revealed that PPARα was recruited to promoter regions of both adipogenic and FA oxidation-related genes in the presence of GW7647 in 3T3-L1 adipocytes. These findings indicate that the activation of PPARα affects energy metabolism in adipocytes, and PPARα activation in WAT may contribute to the clinical effects of fibrate drugs