Acute Effects of Beta-Adrenergic Agonists on Porcine Adipocyte Metabolism In Vitro3

Liu, C. Y.; Boyer, J; Mills, S.E.

doi:10.2527/jas1989.67112930x

Cited by 46 publications

(30 citation statements)

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“…In this study, β-adrenergic stimulation by clenbuterol led to in- creased basal lipolysis and a modest decrease of adipogenesis in adipocytes. This result is consistent with the report showing lipolysis is more sensitive to beta-adrenergic stimulation than is lipogenesis [21]. Beta receptors are linked to Gs proteins, which are in turn linked to adenyl cyclase.…”

Section: Discussionsupporting

confidence: 93%

Effect of clenbuterol on apoptosis, adipogenesis, and lipolysis in adipocytes

et al. 2010

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Clenbuterol, a beta(2)-adrenergic receptor (beta(2)-AR) selective agonist, has been shown to decrease body fat in animals and can induce apoptosis in adipose tissue in mice. We hypothesized that direct actions of a beta-adrenergic receptor agonist on adipocytes could trigger the observed apoptotic effect. The hypothesis was inspected by investigating the direct effect of clenbuterol on apoptosis, adipogenesis, and lipolysis in vitro using the 3T3-L1 cell line and rat primary adipocytes. Cells were treated with 10(-9) to 10(-5) M clenbuterol depending on the experiments. There was no apoptotic effect of clenbuterol both in 3T3-L1 cells and rat primary adipocytes. Adipogenesis monitored by Oil Red O staining and AdipoRed assay was modestly decreased by clenbuterol treatment (p < 0.05). In fully differentiated primary adipocytes, clenbuterol increased basal lipolysis compared with the control (p < 0.01). In summary, direct stimulation of beta(2)-AR by clenbuterol does not cause apoptosis in adipocytes, despite a direct lipolytic stimulation and attenuation of adipogenesis.

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Section: Discussionsupporting

confidence: 93%

Effect of clenbuterol on apoptosis, adipogenesis, and lipolysis in adipocytes

et al. 2010

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“…Adipocytes were isolated from the subcutaneous fat depot of male castrate pigs weighing ϳ100 kg by collagenase digestion as described previously (19,27,28). Briefly, the isolated cells were diluted to approximate 20% cell suspensions with DMEM (Sigma, St. Louis, MO) containing 3% fatty acid-free serum albumin.…”

Section: Methodsmentioning

confidence: 99%

Interleukin-6 and interleukin-15 are selectively regulated by lipopolysaccharide and interferon-γ in primary pig adipocytes

Ajuwon

Jacobi

Kuske

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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3T3-L1 adipocytes express the lipopolysaccharide (LPS) receptor and respond to direct stimulation with the antigen by increasing the expression of inflammatory mediators. Activation of this receptor by its ligand in the macrophage causes the activation and translocation of nuclear factor-kappaB (NF-kappaB) to the nucleus where it regulates the expression of proinflammatory cytokines and other target genes. We investigated whether LPS could stimulate NF-kappaB translocation in primary pig adipocytes and regulate the expression and secretion of TNF-alpha and IL-6. LPS clearly induced the nuclear translocation of NF-kappaB and also upregulated (P < 0.05) the mRNA expression and secretion of IL-6 into the culture medium. An induction of TNF-alpha expression by LPS was not detected, but with extended incubation (8 h), there was a modest increase (P < 0.09) in the media concentration of this cytokine. Inhibition of either ERK1/2, PKC, or the inhibitory G protein (Gi) with U-0126, bisindolylmaleimide HCl, and pertussis toxin, respectively, blocked (P < 0.05) the increase in IL-6 expression caused by LPS. Because LPS administration in vivo increases circulating concentrations of IFN-gamma, and because this cytokine also regulates multiple immune modulators in the adipocyte, we also determined whether IFN-gamma regulates cytokine expression in primary adipocytes. Although the expression of IL-6 and TNF-alpha was unresponsive to IFN-gamma, the expression of IL-15 was markedly upregulated (P < 0.01). Furthermore, the induction of IL-15 expression by IFN-gamma was blocked by inhibition of PKC. These data indicate that NF-kappaB is responsive to LPS in the adipocyte and also identify key mediators of LPS-induced IL-6 expression. In addition, we provide novel evidence that IFN-gamma targets the adipocyte to induce IL-15 expression, thus indicating a possible role for the adipocyte in the regulation of T-cell function and muscle metabolism during the innate immune response.

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“…Nourozi et al (2008) did not observe significant effect on blood glucose and urea contents for ewes with terbutaline and metaproterenol added to the diet. However, Liu et al (1989), and Peterla and Scanes (1990) reported that β-AA such isoproterenol, cimaterol, clenbuterol and ractopamine, have direct effects on porcine adipose tissue in vitro, all decreasing lipogenesis and inhibiting lipid synthesis. Beermann (1987) mentioned that blood metabolites such as plasma free fatty acids and glucose increased sharply after administration of cimaterol, within the first 4to 10 h to then got back to baseline levels, consistent with an acute lipolytic and hyperglycemic effect of β-AA.…”

Section: Serum Metabolitesmentioning

confidence: 96%