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Variability of convective rainfall in the austral summer season over central Madagascar is studied using an area-rainfall index, local radiosonde data, and gridded information on outgoing longwave radiation (OLR), sea-surface temperature, and tropospheric winds. Seasonal rainfall patterns are influenced by topography, monsoon and trade wind circulations, and tropical cyclone events. The Inter Tropical Convergence Zone overlies the north-west coast, where summer rainfall averages 47 cm month-'. Climatic conditions that affect convective rainfall at interannual time-scales are studied through spatial lag correlation analysis. Sea-surface temperature is weakly correlated with rainfall departures, with positive values in the central Indian Ocean reaching +0.41 at lags -4 and 0 months. Strongest positive correlations (+0.45) gradually shift to the central South Atlantic Ocean at lag 0 and +2 months. Wind correlations imply that increased upper level tropical easterly flow overlying enhanced low-level north-west monsoon flow favours above normal rainfall. Regional teleconnection patterns identified by rainfall-OLR correlations are remarkably similar to those for Quasi-biennial oscillation (QBOWLR correlations, suggesting that up to one-third of the interannual convective variance can be explained by the phase of the QBO.

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Protein kinase C epsilon (PKC 3) activation in the liver is proposed to inhibit insulin action through phosphorylation of the insulin receptor. Here, however, we demonstrated that global, but not liver-specific, deletion of PKC 3 in mice protected against dietinduced glucose intolerance and insulin resistance. Furthermore, PKC 3-dependent alterations in insulin receptor phosphorylation were not detected. Adipose-tissue-specific knockout mice did exhibit improved glucose tolerance, but phosphoproteomics revealed no PKC 3-dependent effect on the activation of insulin signaling pathways. Altered phosphorylation of adipocyte proteins associated with cell junctions and endosomes was associated with changes in hepatic expression of several genes linked to glucose homeostasis and lipid metabolism. The primary effect of PKC 3 on glucose homeostasis is, therefore, not exerted directly in the liver as currently posited, and PKC 3 activation in this tissue should be interpreted with caution. However, PKC 3 activity in adipose tissue modulates glucose tolerance and is involved in crosstalk with the liver.

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