Vagal afferents mediate the feeding response to mercaptoacetate but not to the beta (3) adrenergic receptor agonist CL 316,243

Brandt, Karsten; Arnold, Myrtha; Geary, Nori; Langhans, Wolfgang; Leonhardt, M.

doi:10.1016/j.neulet.2006.10.034

Cited by 25 publications

(19 citation statements)

References 26 publications

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“…Peripheral, but not central anorectic effect of isoproterenol is mediated by beta adrenergic receptors. As reported by previous studies these effects are not related to sensory information transmitted via the vagus nerve [7]. The mechanism underlying the beta receptors induced hypophagia is still unclear, although the anorexic effect of beta receptors was reported to be mediated by serotonin but not histamine [8].…”

Section: Introductionsupporting

confidence: 49%

Possible Involvement of Beta-Adrenergic Receptors on Nociceptin/Orphanin FQ Induced Food Consumption in Male Rats

Hajinezhad¹,

Shohreh²

2016

Zahedan J Res Med Sci

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Section: Introductionsupporting

confidence: 49%

Possible Involvement of Beta-Adrenergic Receptors on Nociceptin/Orphanin FQ Induced Food Consumption in Male Rats

Hajinezhad¹,

Shohreh²

2016

Zahedan J Res Med Sci

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“…Other studies also have shown that peripheral administration of PPAR-␣ agonists stimulated intestinal rather than hepatic FAO (49,50). In addition, the FAO inhibitors with an eating-stimulatory effect do require intact abdominal vagal afferents to increase food intake (6,30). Hepatic parenchyma does, however, scarcely contain vagal afferent fibers (2).…”

Section: Discussionmentioning

confidence: 99%

“…The eating-stimulatory effect of MA was associated with a decline in circulating ketone bodies and an increase in nonesterified fatty acids (NEFA), indicating an inhibition of FAO (5, 45). Moreover, FAO inhibitors require intact abdominal vagal afferents to stimulate eating (6,20,29,44), suggesting that they act in the abdominal cavity to do so. Given the major role of the liver in FAO and ketogenesis (38), the eating-stimulatory effect of FAO inhibitors was hypothesized to originate in the liver, with changes in hepatocyte ADP-to-ATP ratio and membrane potential connecting hepatocyte FAO to vagal afferent activity (4,19,27).…”

mentioning

confidence: 99%

Enhancing hepatic mitochondrial fatty acid oxidation stimulates eating in food-deprived mice

Mansouri

Pacheco-López

Ramachandran

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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(FAO) has long been implicated in the control of eating. Nevertheless, direct evidence for a causal relationship between changes in hepatic FAO and changes in food intake is still missing. Here we tested whether increasing hepatic FAO via adenovirusmediated expression of a mutated form of the key regulatory enzyme of mitochondrial FAO carnitine palmitoyltransferase 1A (CPT1mt), which is active but insensitive to inhibition by malonyl-CoA, affects eating and metabolism in mice. CPT1mt expression increased hepatocellular CPT1 protein levels. This resulted in an increase in circulating ketone body levels in fasted CPT1mt-expressing mice, suggesting an increase in hepatic FAO. These mice did not show any significant changes in cumulative food intake, energy expenditure, or respiratory quotient after 4-h food deprivation. After 24-h food deprivation, however, the CPT1mt-expressing mice displayed increased food intake. Thus expression of CPT1mt in the liver increases hepatic FAO capacity, but does not inhibit eating. Rather, it may even stimulate eating after prolonged food deprivation. These data do not support the hypothesis that an increase in hepatic FAO decreases food intake. energy homeostasis; carnitine palmitoyltransferase 1a; food intake; metabolic control of eating; liver BECAUSE FOOD is the only source of metabolic fuels, it is reasonable to assume that feedback from metabolism contributes to the control of eating, allowing for the maintenance of a balance between the amount of calories spent and ingested (52, 53). The nervous system continuously monitors metabolism to assess the availability of energy-providing fuels such as fatty acids and glucose and to control energy intake and expenditure accordingly. Despite open questions concerning its physiological relevance, the eating-stimulatory effect of inhibitors of glucose utilization or fatty acid oxidation (FAO) is generally considered evidence for the existence of a metabolic control of eating (12,27,43). FAO inhibitors such as mercaptoacetate (MA, an inhibitor of acyl-CoA dehydrogenases) (45) and etomoxir or methyl-palmoxirate (inhibitors of the carnitine palmitoyltransferase-1, CPT1) (13,14,19) reliably stimulate eating in laboratory mice (9, 51), rats (5, 19), and humans (18). The eating-stimulatory effect of MA was associated with a decline in circulating ketone bodies and an increase in nonesterified fatty acids (NEFA), indicating an inhibition of FAO (5, 45). Moreover, FAO inhibitors require intact abdominal vagal afferents to stimulate eating (6,20,29,44), suggesting that they act in the abdominal cavity to do so. Given the major role of the liver in FAO and ketogenesis (38), the eating-stimulatory effect of FAO inhibitors was hypothesized to originate in the liver, with changes in hepatocyte ADP-to-ATP ratio and membrane potential connecting hepatocyte FAO to vagal afferent activity (4,19,27). So far, however, all these findings were correlative, and there is no direct evidence supporting the hypothesis that the liver is the organ where the brai...

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“…GLP-1 and PYY are increased in dgat-1 Ϫ / Ϫ mice ( 51 ), and some evidence indicates that pharmacological DGAT-1 inhibition also leads to an enhanced release of these two hormones ( 35,52 ) in addition to the and the observed reduction of food intake after DGAT-1 inhibition. Indeed, hepatic FAO appears to be neither suffi cient nor necessary for the eating-stimulatory effect of the FAO inhibitor mercaptoacetate (MA), but does require intact abdominal vagal afferents ( 49 ), suggesting that the eating-inhibitory effect of MA originates in the intestine.…”

Section: Discussionmentioning

confidence: 99%

Diacylglycerol acyltransferase-1 inhibition enhances intestinal fatty acid oxidation and reduces energy intake in rats

Schober

Arnold

Birtles

et al. 2013

Journal of Lipid Research

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( 1, 2 ). Often an overconsumption of energy-dense, fat-rich food leads to excessive triacylglycerol (TAG) accumulation in adipose and nonadipose tissue. This can result in insulin resistance and nonalcoholic fatty liver disease, emphasizing the need for pharmacotherapeutic approaches that are effective when a high-fat diet (HFD) is consumed ( 3 ).In the small intestine dietary TAGs are hydrolyzed to 2-monoacylglycerols (MAGs) and fatty acids (FAs) that are absorbed . Specifi c binding proteins in the enterocytes shuttle MAG and FFA to the endoplasmic reticulum for reesterifi cation. This involves the acylation from MAG to sn -1,2-diacylglycerol (DAG) by MAG acyltransferase and the acylation from DAG to TAG catalyzed by acyl CoA:diacylglycerol acyltransferase-1 (DGAT-1) (EC 2.3.1.20 ), the rate-limiting step in TAG synthesis ( 4 ). This MAG pathway is important after eating, when intestinal MAG levels are high ( 5 ). DGAT-1 is one of two known DGAT enzymes ( 6 ) in tissues associated with TAG synthesis, including the small intestine ( 6, 7 ), where DGAT-1 is involved in fat absorption, lipoprotein assembly, and regulation of plasma TAG concentrations ( 7 ). DGAT-1 knockout (dgat-1 Obesity is a global epidemic and a major risk factor for type 2 diabetes, hypertension, cardiovascular disease, and other ailments. The development of obesity is multifactorial 28 February 2013. Published, JLR Papers in Press, February 28, 2013 DOI 10.1194 Diacylglycerol acyltransferase-1 inhibition enhances intestinal fatty acid oxidation and reduces energy intake in rats Abbreviations: AMPK ␣ , AMP-activated protein kinase-␣ ; ASP, acid soluble products; AUC, area under the curve; BHB, ␤ -hydroxybutyrate; BT, body temperature; BW, body weight; CFA, conditioned fl avor avoidance; CPT-1, carnitine palmitoyltransferase-1; DAG, sn -1,2-diacylglycerol; DGAT-1, acyl-CoA:diacylglycerol acyltransferase-1; DGAT-1i, diacylglycerol acyltransferase-1 inhibitor; dgat-1 Ϫ / Ϫ This work was supported by Swiss National Science Foundation Grant 31_130665 (W.L.). Manuscript received 19 December 2012 and in revised form

show abstract

Vagal afferents mediate the feeding response to mercaptoacetate but not to the beta (3) adrenergic receptor agonist CL 316,243

Cited by 25 publications

References 26 publications

Possible Involvement of Beta-Adrenergic Receptors on Nociceptin/Orphanin FQ Induced Food Consumption in Male Rats

Possible Involvement of Beta-Adrenergic Receptors on Nociceptin/Orphanin FQ Induced Food Consumption in Male Rats

Enhancing hepatic mitochondrial fatty acid oxidation stimulates eating in food-deprived mice

Diacylglycerol acyltransferase-1 inhibition enhances intestinal fatty acid oxidation and reduces energy intake in rats

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