The obesity epidemic is a growing health, social and economic problem worldwide. Aside from being a social stigma, obesity is frequently associated with insulin resistance, in turn linked to development of type II diabetes, hypertension, hyperlipidemia, and atherosclerosis – the so-called metabolic syndrome (Alberti et al., 2006).
Obesity and metabolic syndrome have earned the name “the silent disease” because their adverse effects are insidious (Abraham et al., 2016). According to World Health Organization (WHO), Obesity is defined as a profuse accumulation of fat caused by an imbalance in intake and consumption of energy accompanied by insufficient physical activity (WHO, 2017).
Obesity is considered as a complex neuroendocrine disorder in which genetic predisposition and environmental factors act in concern (Walley et al., 2009, and Hebebrand et al, 2009). The brain plays a relevant role in the regulation of appetite, body weight, and physical activity. The hypothalamus [via regulatory neuropeptides such as cholecystokinin, ghrelin, neuropeptide Y] is a brain region that chiefly regulates hemostasis food intake (Dietrich et al, 2009) and is implicated in obesity (Belgardt et al., 2009). Also, Adipocytes secrete a variety of bioactive peptide hormones called adipokines [e.g. leptin, adiponectin, resistin, visfatin, tumor necrosis factor-α (TNF-α) and interleukin (IL)-6], which play a role in energy regulation (Garg, 2006). A unifying mechanism behind the pathogenesis of obesity-associated diseases has given birth of the concept of "meta-inflammation" which describes the chronic low grade inflammatory response to obesity (Lumeng et al, 2011).WNT-inducible signaling pathway protein-1(WISP1), also known as CCN4, is a novel adipokine which is a member of secreted extracellular matrix-associated proteins of the CCN family and a target gene of Wingless type (WNT) signaling pathway. Growing evidence links the WNT signaling pathway to the regulation of adipogenesis and meta-inflammation in obesity (Murahovschi et al., 2015).
WNT signaling family members are secreted glycoproteins that act in both autocrine and paracrine fashions to regulate cell proliferation, cell fate and differentiation (Logan et al, 2004).
The WNT signaling network comprises multiple so-called "canonical' and "non-canonical" pathways that lead to tightly controlled cell remodeling. WISP1 is a downstream target gene of the non-canonical WNT signaling pathway (Katoh et al, 2007) and acts anti-apoptotically through the phosphatidyl-inositol 3-kinase (PIK) and Akt pathways (Maiese et al., 2012).
Heme oxygenase-1 (HO1), the rate-limiting enzyme (EC 18.104.22.168) in heme degradation, catalyzes the oxidation of heme to generate several biologically active molecules: carbon monoxide, biliverdin, and ferrous ion (Maines, 1988). Li et al. (2007) reported that induction of HO1 enhances cell survival and moderates diabetes and obesity. Furthermore, Vanella et al. (2013) showed that increased HO1 expression and activity decreased adipocyte hypertrophy and TNF-α level, and increased adiponectin level and expression of the genes central to the canonical WNT signaling cascade. HO1 acted as upstream regulator of canonical WNT signaling cascade decreasing lipogenesis and adipocyte differentiation.The medicinal properties of ginger have been used since ancient times in India for various biomedical applications especially obesity. Ginger (Zingiber officinale) is the rhizome of the plant, which belongs to the family Zingiberaceae, and is consumed as a medicine or spice (Ali et al., 2008).
The major chemical constituents of the ginger rhizome include a volatile oil and non-volatile pungent compounds e.g. gingerols, shagols and zingerones (Tapsell et al., 2006). Various well-reported pharmacological activities of ginger and its constituents include anti-ulcer, antiplatelet, hypotensive and hypolipidemic actions (González-Castejón et al, 2011).