Bioactive phloroglucinols from the brown alga Zonaria diesingiana

Three phloroglucinols with a C-20 acyl side chain were isolated from marine brown alga Zonaria diesingiana. The structures were determined on the basis of NMR spectral analyses and comparison with data in the literature. They all showed antibacterial activity against Bacillus subtilis and Staphylococcus aureus and cytotoxic activity by inhibiting cell division in fertilized sea urchin eggs (Echinometra mathaei). These activities suggest their possible for pharmacological purposes. These phloroglucinols also showed toxicity against brine shrimp (Artemia salina), guppy fish (Poecilia reticulata), rice-land shrimp (Macrobrachium lanchesteri) and the diatom Chaetoceros gracilis. They probably act as chemical defenses against herbivores and also reduce surface fouling by epiphytic algae and larvae, suggesting their important roles in the marine ecosystem.     

Effect of acute exercise on glycogen synthase in muscle from obese and diabetic subjects

Insulin stimulates glycogen synthase (GS) through dephosphorylation of serine residues, and this effect is impaired in skeletal muscle from insulin-resistant [obese and type 2 diabetic (T2DM)] subjects. Exercise also increases GS activity, yet it is not known whether the ability of exercise to affect GS is impaired in insulin-resistant subjects. The objective of this study was to examine the effect of acute exercise on GS phosphorylation and enzyme kinetic properties in muscle from insulin-resistant individuals. Lean normal glucose-tolerant (NGT), obese NGT, and obese T2DM subjects performed 40 min of moderate-intensity cycle exercise (70% of Vo(2max)). GS kinetic properties and phosphorylation were measured in vastus lateralis muscle before exercise, immediately after exercise, and 3.5 h postexercise. In lean subjects, GS fractional activity increased twofold after 40 min of exercise, and it remained elevated after the 3.5-h rest period. Importantly, exercise also decreased GS K(m) for UDP-glucose from ≈0.5 to ≈0.2 mM. In lean subjects, exercise caused significant dephosphorylation of GS by 50-70% (Ser(641), Ser(645), and Ser(645,649,653,657)), and phosphorylation of these sites remained decreased after 3.5 h; Ser? phosphorylation was not regulated by exercise. In obese NGT and T2DM subjects, exercise increased GS fractional activity, decreased K(m) for UDP-glucose, and decreased GS phosphorylation as effectively as in lean NGT subjects. We conclude that the molecular regulatory process by which exercise promotes glycogen synthesis in muscle is preserved in insulin-resistant subjects.