Going deep into Obesity issues and tumor induced cachexia, we stumble upon RIP 140, Sp1, and believe or not E2F1(a wild gene).
"RIP140 is part of the chain by which tumors can cause cachexia.[15][16]
Levels of RIP140 expression in various tissues varies during aging in mice, suggesting changes in metabolic function.[17]
RIP140 is implicated in certain human disease processes. In morbid
obesity, RIP140 levels are down-regulated in visceral adipose tissue.[18]
In breast cancer, RIP140 is involved in regulation of E2F1, an oncogene
which discriminates between luminal and basal types of tumours. RIP140
has an influence upon cancer phenotype and prognosis.[19] In addition, RIP140 has a role in inflammation, since it acts as a coactivator for NFkappaB/RelA-dependent cytokine gene expression. Lack of RIP140 leads to an inhibition of proinflammatory pathways in macrophages."
wikipedia
It seems that this is where Obesity becomes a disease by its state of high inflammatory state. The diease process in Obesity is defined or determined by a relatively high level of Growth factor and Cytokines inducing major deleterious consequences on the muscle skeletal system through the activated NF-KB. The RIP 140 (also known as NRIP1) is hard at work. Remember it interacts with DAX1 which involves the COPS2 (nothing to do with the police!),SREBF1 (the bone modulator) and SF1 ("feminization" of the obese individual).
It is clearly important that the understanding and measurement of the obese by clear new biomarkers allow us to establish new guidelines for monitoring. Following BMI, lipid profile and pushing diet is clearly insufficient. Blocking the central Nervous system to force mental rejection of food is not the only answer ...remember RIP-140 modulation is part of cachexia induced by Tumors.
(remember the rule, if it can induce a malformation, it is an important gene (check out DAX1 and SREBF1)
Othre gene in the link TRERF1, CREB-binding protein,EP 300.
Get to work! At CRBCM...the race is on!
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