Curcumin (diferuloyl methane), a small-molecular weight compound isolated from the roots of Curcuma longa L. (family Zingiberaceae), has been used traditionally for centuries in Asia for medicinal, culinary and other purposes. A large number of in vitro and in vivo studies in both animals and man have indicated that curcumin has strong antioxidant, anti-carcinogenic, anti-inflammatory, anti-angiogenic, antispasmodic, antimicrobial, anti-parasitic and other activities. The mechanisms of some of these actions have recently been intensively investigated. Curcumin inhibits the promotion/ progression stage of carcinogenesis by induction of apoptosis and the arrest of cancer cells in the S, G2/M cell cycle phase. The compound inhibits the activity of growth factor receptors. The anti-inflammatory properties of curcumin are mediated through their effects on cytokines, lipid mediators, eicosanoids and proteolytic enzymes. Curcumin scavenges the superoxide radical, hydrogen peroxide and nitric oxide, and inhibits lipid peroxidation. These actions may be the basis for many of its pharmacological and therapeutic properties. Curcumin is a nutraceutical of low toxicity, which has been used successfully in a number of medical conditions that include cataracts, cystic fibrosis, and prostate and colon cancers.

Uncertainty reigns over whether or not glutamate uptake in astrocytes leads to strong stimulation of glucose utilization, measured as accumulation of radioactive deoxyglucose-6-phosphate. This is an important issue, not only because glutamate is the major excitatory transmitter, but also because it has been postulated that glutamate-induced stimulation of glycolysis links brain excitation with activation of energy production. The effect of glutamate on deoxyglucose utilization in cultured rat and mouse astrocytes grown in different media and incubated under various conditions during the deoxyglucose assay has, therefore, been studied. Under most conditions, no stimulation occurred but rather a decrease in deoxyglucose utilization during exposure to glutamate; under certain conditions, the contribution of non-metabolized deoxyglucose to the intracellular ¹⁴C signal was significant.

We studied temperature homeostasis in male mice lacking all thyroid hormone receptor-alpha gene products (TRalpha-0/0). As other TRalpha-deficient mice, TRalpha-0/0 mice have lower core body temperature (T(C)) than cognate wild-type controls. We found that obligatory thermogenesis is normal in TRalpha-0/0 and that the lower T(C) at room temperature (RT, 20-22 C) is caused by a down setting of the hypothalamic thermostat. However, TRalpha-0/0 mice are cold intolerant due to impaired facultative thermogenesis. Norepinephrine-induced brown adipose tissue (BAT) thermogenesis is blunted, even though BAT-relevant genes and T(4) deiodinase respond normally to cold stimulation, as do serum T(3), serum glycerol (marker of lipolysis), and heart rate. BAT normally contributes to maintain T(C) at RT, 9 C below thermoneutrality, yet TRalpha-0/0 mice do not show signs of being cold stressed at 20-22 C. Instead, oxygen consumption is greater in TRalpha-0/0 than in wild-type mice at RT, suggesting the recruitment of an alternate, cold-activated form of thermogenesis to compensate for the lack of BAT thermogenesis. These results indicate that TRalpha is necessary for T(3) to modulate the central control of T(C) and for an essential step in norepinephrine activation of BAT thermogenesis but not to sustain obligatory thermogenesis. In addition, the results provide evidence for an alternate form of facultative thermogenesis, which probably originates in skeletal muscle and that is less effective and more energy demanding than BAT thermogenesis.