“…TNFα is an inflammatory cytokine released by adipose tissue and is becoming recognised as an important component of normal energy homeostasis (Pamir et al, 2009; Endo et al, 2007). It has long been known that elevated TNFα might be an important component of the depressed appetite in disease and infection states (Langhans and Hrupka, 1999; Plata-Salaman et al, 1996; Sonti et al, 1996), such as cancer cachexia (Argiles et al, 2003; Argiles et al, 2005; Bernstein, 1996; Bernstein et al, 1991; Langstein et al, 1991; Smith and Kluger, 1993; Tisdale, 1999), Crohn’s disease (Diamanti et al, 2009), chronic obstructive pulmonary disease (Calikoglu et al, 2004) and infection (Truyens et al, 1995), as well as the anorexia induced by lipopolysaccharide injection (Arsenijevic et al, 2000; Kim et al, 2007; Porter et al, 1998; Tollner et al, 2000). Mice with the TNFα converting enzyme (TACE; also known as ADAM17) inactivated are hypermetabolic and lean (Gelling et al, 2008), whereas those with both TNF receptors knocked out are obese and insulin resistant (Pamir et al, 2009).…”