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An important regulator of fatty acid oxidation (FAO) is the allosteric inhibition of CPT-1 by malonyl-CoA produced by the enzyme acetyl-CoA carboxylase 2 (ACC2). Initial studies suggested that deletion of Acc2 (Acacb) increased fat oxidation and reduced adipose tissue mass but in an independently generated strain of Acc2 knockout mice we observed increased whole-body and skeletal muscle FAO and a compensatory increase in muscle glycogen stores without changes in glucose tolerance, energy expenditure or fat mass in young mice (12-16 weeks). The aim of the present study was to determine whether there was any effect of age or housing at thermoneutrality (29°C; which reduces total energy expenditure) on the phenotype of Acc2 knockout mice. At 42-54 weeks of age, male WT and Acc2-/- mice had similar body weight, fat mass, muscle triglyceride content and glucose tolerance. Consistent with younger Acc2-/- mice, aged Acc2-/- mice showed increased whole-body FAO (24 h average respiratory exchange ratioZ0.95±0.02 and 0.92±0.02 for WT and Acc2-/- mice respectively, P<0.05) and skeletal muscle glycogen content (C60%, P<0.05) without any detectable change in whole-body energy expenditure. Hyperinsulinaemic- euglycaemic clamp studies revealed no difference in insulin action between groups with similar glucose infusion rates and tissue glucose uptake. Housing Acc2-/- mice at 29°C did not alter body composition, glucose tolerance or the effects of fat feeding compared with WT mice. These results confirm that manipulation of Acc2 may alter FAO in mice, but this has little impact on body composition or insulin action. [ABSTRACT FROM AUTHOR]

Parkin is an E3-ubiquitin ligase belonging to the RBR (RING-InBetweenRING-RING family), and is involved in the neurodegenerative disorder Parkinson's disease. Autosomal recessive juvenile Parkinsonism, which is one of the most common familial forms of the disease, is directly linked to mutations in the parkin gene. However, the molecular mechanisms of Parkin dysfunction in the disease state remain to be established. We now demonstrate that the ubiquitin-like domain of Parkin functions to inhibit its autoubiquitination. Moreover pathogenic Parkin mutations disrupt this autoinhibition, resulting in a constitutively active molecule. In addition, we show that the mechanism of autoregulation involves ubiquitin binding by a C-terminal region of Parkin. Our observations provide important molecular insights into the underlying basis of Parkinson's disease, and in the regulation of RBR E3-ligase activity. [ABSTRACT FROM AUTHOR]

An abstract of the article "Metabolic defects induced by high-fat feeding in mice are rapidly reversed by a low-fat diet," by Nigel Turner, Simon J. Leslie, Nicole L. Hallahan, and Gregory J. Cooney is presented.

An important regulator of fatty acid oxidation (FAO) is the allosteric inhibition of CPT-1 by malonyl-CoA produced by the enzyme acetyl-CoA carboxylase 2 (ACC2). Initial studies suggested that deletion of Acc2 (Acacb) increased fat oxidation and reduced adipose tissue mass but in an independently generated strain of Acc2 knockout mice we observed increased whole-body and skeletal muscle FAO and a compensatory increase in muscle glycogen stores without changes in glucose tolerance, energy expenditure or fat mass in young mice (12-16 weeks). The aim of the present study was to determine whether there was any effect of age or housing at thermoneutrality (29 °C; which reduces total energy expenditure) on the phenotype of Acc2 knockout mice. At 42-54 weeks of age, male WT and Acc2(-/-) mice had similar body weight, fat mass, muscle triglyceride content and glucose tolerance. Consistent with younger Acc2(-/-) mice, aged Acc2(-/-) mice showed increased whole-body FAO (24 h average respiratory exchange ratio=0.95±0.02 and 0.92±0.02 for WT and Acc2(-/-) mice respectively, P<0.05) and skeletal muscle glycogen content (+60%, P<0.05) without any detectable change in whole-body energy expenditure. Hyperinsulinaemic-euglycaemic clamp studies revealed no difference in insulin action between groups with similar glucose infusion rates and tissue glucose uptake. Housing Acc2(-/-) mice at 29 °C did not alter body composition, glucose tolerance or the effects of fat feeding compared with WT mice. These results confirm that manipulation of Acc2 may alter FAO in mice, but this has little impact on body composition or insulin action., (© 2016 Society for Endocrinology.)

Antarctic mosses live in a frozen desert, and are characterised by the ability to survive desiccation. They can tolerate multiple desiccation-rehydration events over the summer growing season. As a result of recent ozone depletion, such mosses may also be exposed to ultraviolet-B radiation while desiccated. The ultraviolet-B susceptibility of Antarctic moss species was examined in a laboratory experiment that tested whether desiccated or hydrated mosses accumulated more DNA damage under enhanced ultraviolet-B radiation. Accumulation of cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrimidone dimers was measured in moss samples collected from the field and then exposed to ultraviolet-B radiation in either a desiccated or hydrated state. Two cosmopolitan species, Ceratodon purpureus (Hedw.) Brid. and Bryum pseudotriquetrum (Hedw.) Gaertn., B.Mey. & Scherb, were protected from DNA damage when desiccated, with accumulation of cyclobutane pyrimidine dimers reduced by at least 60% relative to hydrated moss. The endemic Schistidium antarctici (Cardot) L.I. Savicz & Smirnova accumulated more DNA damage than the other species and desiccation was not protective in this species. The cosmopolitan species remarkable ability to tolerate high ultraviolet-B exposure, especially in the desiccated state, suggests they may be better able to tolerate continued elevated ultraviolet-B radiation than the endemic species.