Effects of pertussis toxin treatment on the metabolism of rat adipocytes.

Moreno, Francisco J.; Mills, Ira; García‐Sáinz, J. Adolfo; Fain, John N.

doi:10.1016/s0021-9258(17)44366-3

Cited by 109 publications

(6 citation statements)

References 25 publications

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“…Mice deficient in GPR43 do not display an overt phenotype when fed a chow diet [53,113]. Acetate and G i/o signaling have been shown to suppress lipolysis both in vitro and in vivo [53,[114][115][116]-an effect that was blunted in GPR43-KO mice [113]. When fed an HFD, no differences in body weight or composition were noted until 26 weeks of age, at which point GPR43-KO mice were leaner and weighed less than their wild-type counterparts, likely due to increased energy expenditure [113].…”

Section: Gpr43mentioning

confidence: 99%

Modulation of Adipocyte Metabolism by Microbial Short-Chain Fatty Acids

May

Hartigh

2021

Nutrients

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Obesity and its complications—including type 2 diabetes, cardiovascular disease, and certain cancers—constitute a rising global epidemic that has imposed a substantial burden on health and healthcare systems over the years. It is becoming increasingly clear that there is a link between obesity and the gut microbiota. Gut dysbiosis, characterized as microbial imbalance, has been consistently associated with obesity in both humans and animal models, and can be reversed with weight loss. Emerging evidence has shown that microbial-derived metabolites such as short-chain fatty acids (SCFAs)—including acetate, propionate, and butyrate—provide benefits to the host by impacting organs beyond the gut, including adipose tissue. In this review, we summarize what is currently known regarding the specific mechanisms that link gut-microbial-derived SCFAs with adipose tissue metabolism, such as adipogenesis, lipolysis, and inflammation. In addition, we explore indirect mechanisms by which SCFAs can modulate adipose tissue metabolism, such as via perturbation of gut hormones, as well as signaling to the brain and the liver. Understanding how the modulation of gut microbial metabolites such as SCFAs can impact adipose tissue function could lead to novel therapeutic strategies for the prevention and treatment of obesity.

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Section: Gpr43mentioning

confidence: 99%

Modulation of Adipocyte Metabolism by Microbial Short-Chain Fatty Acids

May

Hartigh

2021

Nutrients

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“…The Bordetella pertussis exotoxin is reported to catalyse the ADP-ribosylation of the Mr-41 000 ax-subunit of Ni (Bokoch et al, 1984;Codina et al, 1984) and thereby to attenuate the effect of inhibitory agonists that are normally coupled to adenylate cyclase through this protein (Moreno et al, 1983;Olansky et al, 1983). We are unaware of any investigations using pertussis toxin in brown adipose tissue.…”

Section: Effect Of Pertussis Toxinmentioning

confidence: 99%

“…In white adipose tissue, lipolysis, besides being increased by stimulatory agonists such as the catecholamine hormones, is also decreased by inhibitory agonists such as adenosine, E-series prostaglandins and nicotinic acid. Receptors for these inhibitory agonists appear to be coupled to adenylate cyclase by a guanine-nucleotidebinding protein (N1) distinct from that (N.) which couples receptors for stimulatory agonists to the enzyme (Rodbell, 1980;Murayama & Ui, 1983;Olansky et al, 1983;Moreno et al, 1983;Bokoch et al, 1984;Codina et al, 1984). This inhibitory action of adenosine is mediated by the A1 (Van Calker et al, 1979) or R1 (Londos et al, 1980) type of adenosine receptor.…”

Section: Introductionmentioning

confidence: 99%

Effect of adenosine deaminase, N6-phenylisopropyladenosine and hypothyroidism on the responsiveness of rat brown adipocytes to noradrenaline

Woodward¹,

Saggerson²

1986

Biochemical Journal

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Adenosine deaminase (1 unit/ml) potentiated the lipolytic action of noradrenaline in adipocytes isolated from brown adipose tissue of 1- and 6-week-old rats by decreasing the EC50 (concn. giving 50% of maximal effect) for noradrenaline by 3-4-fold. With cells from neonatal rabbit tissue, adenosine deaminase only had a small, non-significant, effect on the EC50 for noradrenaline. Lipolysis in rat brown adipocytes was inhibited by low concentrations of N6-phenylisopropyladenosine (PIA). Rabbit cells were far less sensitive to PIA. PIA, prostaglandin E1 and nicotinate all inhibited noradrenaline-stimulated respiration in rat brown adipocytes. Hypothyroidism diminished the maximum response of respiration and lipolysis to noradrenaline in rat cells and increased the EC50 for noradrenaline. Responsiveness of lipolysis to noradrenaline was particularly decreased in hypothyroidism and was partially restored by addition of adenosine deaminase. Lipolysis in cells from hypothyroid rats was more sensitive to the anti-lipolytic action of PIA. Bordetella pertussis toxin increased lipolysis in the presence of PIA, suggesting an involvement of the Ni guanine-nucleotide-binding protein in the control of brown-adipocyte metabolism.

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“…Bordetella pertussis toxin ("islet-activating protein"), an etiologic agent in pertussis or whooping cough, catalyzes the ADP-ribosylation of Gio (Katada & Ui, 1982a,b;Bokoch et al, 1983;Codina et al, 1983). Modification of Gio results in the "uncoupling" of G| from inhibitory hormone receptors (Kurose et al, 1983;Hsia et al, 1984a); the effect of toxin-catalyzed ADPribosylation of G, is a loss of inhibitory agonist action, permitting unopposed activity of the stimulatory arm of the cyclase system (Katada & Ui, 1982a,b;Moreno et al, 1983;Hsia et al. 1984b).…”

mentioning

confidence: 99%

Stimulation of the thiol-dependent ADP-ribosyltransferase and NAD glycohydrolase activities of Bordetella pertussis toxin by adenine nucleotides, phospholipids, and detergents

Moss¹,

Stanley²,

Watkins³

et al. 1986

Biochemistry

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Pertussis toxin catalyzed ADP-ribosylation of the guanyl nucleotide binding protein transducin was stimulated by adenine nucleotide and either phospholipids or detergents. To determine the sites of action of these agents, their effects were examined on the transducin-independent NAD glycohydrolase activity. Toxin-catalyzed NAD hydrolysis was increased synergistically by ATP and detergents or phospholipids; the zwitterionic detergent 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate (CHAPS) was more effective than the nonionic detergent Triton X-100 greater than lysophosphatidylcholine greater than phosphatidylcholine. The A0.5 for ATP in the presence of CHAPS was 2.6 microM; significantly higher concentrations of ATP were required for maximal activation in the presence of cholate or lysophosphatidylcholine. In CHAPS, NAD hydrolysis was enhanced by ATP greater than ADP greater than AMP greater than adenosine; ATP was more effective than MgATP or the nonhydrolyzable analogue adenyl-5'-yl imidodiphosphate. GTP and guanyl-5'-yl imidodiphosphate were less active than the corresponding adenine nucleotides. Activity in the presence of CHAPS and ATP was almost completely dependent on dithiothreitol; the A0.5 for dithiothreitol was significantly decreased by CHAPS alone and, to a greater extent, by CHAPS and ATP. To determine the site of action of ATP, CHAPS, and dithiothreitol, the enzymatic (S1) and binding components (B oligomer) were resolved by chromatography. The purified S1 subunit catalyzed the dithiothreitol-dependent hydrolysis of NAD; activity was enhanced by CHAPS but not ATP. The studies are consistent with the conclusion that adenine nucleotides, dithiothreitol, and CHAPS act on the toxin itself rather than on the substrate; adenine nucleotides appear to be involved in the activation of toxin but not the isolated catalytic unit.

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Effects of pertussis toxin treatment on the metabolism of rat adipocytes.

Cited by 109 publications

References 25 publications

Modulation of Adipocyte Metabolism by Microbial Short-Chain Fatty Acids

Modulation of Adipocyte Metabolism by Microbial Short-Chain Fatty Acids

Effect of adenosine deaminase, N6-phenylisopropyladenosine and hypothyroidism on the responsiveness of rat brown adipocytes to noradrenaline

Stimulation of the thiol-dependent ADP-ribosyltransferase and NAD glycohydrolase activities of Bordetella pertussis toxin by adenine nucleotides, phospholipids, and detergents

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