G-1, Appeal Activity In The Public Assistance Programs, November 2004

Appeal Activity In The Public Assistance Programs

NCoR1 is a conserved physiological modulator of muscle mass and oxidative function.

Transcriptional coregulators control the activity of many transcription factors and are thought to have wide-ranging effects on gene expression patterns. We show here that muscle-specific loss of nuclear receptor corepressor 1 (NCoR1) in mice leads to enhanced exercise endurance due to an increase of both muscle mass and of mitochondrial number and activity. The activation of selected transcription factors that control muscle function, such as MEF2, PPARβ/δ, and ERRs, underpins these phenotypic alterations. NCoR1 levels are decreased in conditions that require fat oxidation, resetting transcriptional programs to boost oxidative metabolism. Knockdown of gei-8, the sole C. elegans NCoR homolog, also robustly increased muscle mitochondria and respiration, suggesting conservation of NCoR1 function. Collectively, our data suggest that NCoR1 plays an adaptive role in muscle physiology and that interference with NCoR1 action could be used to improve muscle function.

Altered growth in male peroxisome proliferator-activated receptor gamma (PPARgamma) heterozygous mice: involvement of PPARgamma in a negative feedback regulation of growth hormone action.

The peroxisome proliferator-activated receptor gamma (PPARgamma) plays a major role in fat tissue development and physiology. Mutations in the gene encoding this receptor have been associated to disorders in lipid metabolism. A thorough investigation of mice in which one PPARgamma allele has been mutated reveals that male PPARgamma heterozygous (PPARgamma +/-) mice exhibit a reduced body size associated with decreased body weight, reflecting lean mass reduction. This phenotype is reproduced when treating the mice with a PPARgamma- specific antagonist. Monosodium glutamate treatment, which induces weight gain and alters body growth in wild-type mice, further aggravates the growth defect of PPARgamma +/- mice. The levels of circulating GH and that of its downstream effector, IGF-I, are not altered in mutant mice. However, the IGF-I mRNA level is decreased in white adipose tissue (WAT) of PPARgamma +/- mice and is not changed by acute administration of recombinant human GH, suggesting an altered GH action in the mutant animals. Importantly, expression of the gene encoding the suppressor of cytokine signaling-2, which is an essential negative regulator of GH signaling, is strongly increased in the WAT of PPARgamma +/- mice. Although the relationship between the altered GH signaling in WAT and reduced body size remains unclear, our results suggest a novel role of PPARgamma in GH signaling, which might contribute to the metabolic disorder affecting insulin signaling in PPARgamma mutant mice.

G-1 Appeal Activity In The Public Assistance Programs, December 2004

Appeal Activity In The Public Assistance Programs

Lottery Action, November 15-28, 2004, Vol. 11, no. 12

Iowa Lottery Retailer Newsletter

Lottery Action, November 21 - December 12, 2004, Vol. 11, no 22

Lottery Newsletter for Lottery Retailers

Lottery Action, December 13, 2004 - January 2, 2005, Vol. 11, no. 23

Iowa Lottery Newsletter for Retailers

Lottery Action, January 3-23, 2005, vol. 12, no. 1

Iowa Lottery Newsletter for Retailers

Lottery Action, January 26 - February 6, 2005, Vol. 12, No. 2

Iowa Lottery Newsletter for Retailers

G-1 Appeal Activity In The Public Assistance Programs, January 2005

Appeal Activity In The Public Assistance Programs

Lottery Action, February 7-20, 2005, Vol. 12, no. 3

Iowa Lottery newsletter for Lottery retailers.

Lottery Action, February 21-March 6, 2005, Vol. 12, no. 4

Iowa Lottery Newsletter for Lottery Retailers

Lottery Action, March 3-7, 2005, Vol. 12, no. 5

Lottery Newsletter for Retailers