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  • br Introduction Adipose tissue AT in addition to its

    2022-07-13


    Introduction Adipose tissue (AT), in addition to its function as gstp1-1 storage, is an important endocrine organ and it secretes adipokines (Ahima, 2006). Adipose tissue is related to different physiological processes such as energy metabolism, insulin sensitivity, and inflammation. One important trigger of these effects is the adipokine adiponectin (AdipoQ). Its expression is higher in human visceral (v.c.) adipocytes than in subcutaneous (s.c.) adipocytes in vitro (Motoshima et al., 2002), as was observed for AdipoQ mRNA in rat v.c. compared with s.c. AT (Atzmon et al., 2002). In pigs, AdipoQ expression is related to genotype; a lean pig breed has higher serum concentrations of AdipoQ than a breed with potential for higher fat accretion (Jacobi et al., 2004). Adiponectin improves insulin sensitivity by enhancing glucose uptake and β-oxidation and decreasing gluconeogenesis in liver or muscle (Berg et al., 2001; Fruebis et al., 2001; Yamauchi et al., 2007). As discussed by Brochu-Gaudreau et al. (2010), AdipoQ might protect against fatty liver disease. For this reason, insights into the AdipoQ system in cattle should be of great importance because negative energy balance during transition from late pregnancy to early lactation of dairy cows is often associated with metabolic disorders such as fatty liver disease and ketosis (LeBlanc, 2010). Overexpression of AdipoQ in mice reduces BW in both sexes as well as NEFA in male transgenic mice. In these transgenic mice, AdipoQ diminishes adipocyte differentiation and leads to a larger number of small adipocytes (Bauche et al., 2007). In isolated porcine adipocytes, in vitro AdipoQ reduces lipogenic activity (Jacobi et al., 2004). In contrast, another transgenic mice model describes the proliferation and increase of tissue mass of defined fat pads (Combs et al., 2004). This study was in line with the observation of other investigators showing that AdipoQ overexpression pushes proliferation and differentiation of 3T3-L1 adipocytes and enhances lipid accumulation (Fu et al., 2005). Adiponectin signals through the AdipoQ receptors 1 (AdipoR1) and 2 (AdipoR2), which are the major receptors. The mRNA of the receptor AdipoR1 is ubiquitously expressed and highly abundant in skeletal muscle, whereas that of AdipoR2 is found predominantly in mouse liver (Kadowaki et al., 2006). Both receptors are expressed in AT and downregulated in AdipoQ-overexpressing 3T3-L1 adipocytes (Fu et al., 2005). Downregulation of AdipoR2, but not AdipoR1, was also shown in an AdipoQ-overexpressing transgenic mice model analyzing inguinal and gonadal AT (Bauche et al., 2006). Stimulation of pig adipocytes with insulin alone reduces AdipoQ and AdipoR2 mRNA in vitro (Liu et al., 2008) but increases AdipoQ in 3T3-L1 adipocytes (Scherer et al., 1995). Adiponectin phosphorylates and thereby activates the 5′-AMP-activated protein kinase (AMPK) pathway, which triggers increased fatty acid oxidation, decreases gluconeogenesis, and decreases glucose uptake in muscle or liver (Yamauchi et al., 2002; Guerre-Millo, 2008). For AMPK in AT, the data related to pro- and antilipolytic effects are contradictory (Yin et al., 2003; Daval et al., 2005). Comparable to AMPK, the G-protein coupled receptor 109A (GPR109A; newly named HCA2) is involved in lipolysis; activation of the receptor results in a decrease in lipolysis. The receptor belongs to the family of hydroxy-carboxylic acid receptors and is activated by niacin as well by BHBA as the endogenous ligand (Offermanns et al., 2011). Reduction of lipolysis by BHBA is thought to be an important negative feedback mechanism during starvation (Gille et al., 2008). In dairy cattle, comparable abundance of the receptor protein was found in liver and in kidney fat but most receptor mRNA was observed in liver (Titgemeyer et al., 2011a). The GPR109A mRNA is downregulated during the transition period in s.c. AT of dairy cattle (Lemor et al., 2009). Less information compared with monogastrics is available about the AdipoQ system in general and its relation to genetic background in the bovine species. Adiponectin mRNA was negatively correlated with back fat thickness in Hereford × Aberdeen Angus as well as in Charolais × Red Angus crossbred steers (Taniguchi et al., 2008). An animal model with differences in fat accretion but shared genetic background could be an important tool in understanding the AdipoQ system in cattle. We established such a model, which comprised a segregating F2 family structure using the founder breeds Charolais (accretion-type) and German Holstein (secretion-type) by mating Charolais bulls to German Holstein cows to obtain full-sib and half-sib F2 cows from F1 intercrosses (Kühn et al., 2002). Differences in milk production, body composition, and glucose metabolism were observed. Cows of the F2 family that secrete more milk have less fat content in s.c. and v.c. fat depots, a longer glucose half-life, lesser insulin secretion during oral glucose tolerance test, and higher NEFA concentrations compared with cows of the family that secrete less milk and accrete more fat (Hammon et al., 2010). The higher fat deposition in the cow family that accretes more fat might be related to higher insulin concentrations. Insulin diminishes fatty acid oxidation, increases fatty acid esterification in liver (Zammit, 1996), and stimulates lipogenesis in cattle (Etherton and Evock, 1986).