Glucose‐Responsive Neurons In the Brainstem

Adachi, Akira; Kobashi, Motoi; Funahashi, Makoto

doi:10.1002/j.1550-8528.1995.tb00493.x

Cited by 83 publications

(53 citation statements)

References 13 publications

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“…NPY in the amygdala is linked to anxiolytic-like effects (44); thus the unchanged NPY levels here might indicate no change in stress or anxiety responses across groups. The nucleus of solitary tract in the medulla receives afferent inputs from the vagus nerve arising from the gastrointestinal tract, transferring peripheral satiety signals (1,16,57). The increased medullary NPY concentration induced by either HFD feeding or cigarette smoke exposure alone might reflect altered peripheral input in response to altered feeding states or direct effects of nicotine or some other component of cigarette smoke.…”

Section: Discussionmentioning

confidence: 99%

Detrimental metabolic effects of combining long-term cigarette smoke exposure and high-fat diet in mice

Chen¹,

Hansen²,

Jones³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Morris MJ. Detrimental metabolic effects of combining long-term cigarette smoke exposure and high-fat diet in mice. Am J Physiol Endocrinol Metab 293: E1564-E1571, 2007. First published October 16, 2007 doi:10.1152/ajpendo.00442.2007.-Obesity and cigarette smoking are both important risk factors for insulin resistance, cardiovascular disease, and cancer. Smoking reduces appetite, which makes many people reluctant to quit. Few studies have documented the metabolic impact of combined smoke exposure (se) and high-fat-diet (HFD). Neuropeptide Y (NPY) is a powerful hypothalamic feeding stimulator that promotes obesity. We investigated how chronic se affects caloric intake, adiposity, plasma hormones, inflammatory mediators, and hypothalamic NPY peptide in animals fed a palatable HFD. Balb/c mice (5 wk old, male) were exposed to smoke (2 cigarettes, twice/day, 6 days/wk, for 7 wk) with or without HFD. Sham-exposed mice were handled similarly without se. Plasma leptin, hypothalamic NPY, and adipose triglyceride lipase (ATGL) mRNA were measured. HFD induced a 2.3-fold increase in caloric intake, increased adiposity, and glucose in both sham and se cohorts. Smoke exposure decreased caloric intake by 23%, with reduced body weight in both dietary groups. Fat mass and glucose were reduced only by se in the chow-fed animals. ATGL mRNA was reduced by HFD in se animals. Total hypothalamic NPY was reduced by HFD, but only in sham-exposed animals; se increased arcuate NPY. We conclude that although se ameliorated hyperphagia and reversed the weight gain associated with HFD, it failed to reverse fat accumulation and hyperglycemia. The reduced ATGL mRNA expression induced by combined HFD and se may contribute to fat retention. Our data support a powerful health message that smoking in the presence of an unhealthy Western diet increases metabolic disorders and fat accumulation. adipose triglyceride lipase; appetite; leptin; neuropeptide Y; tumor necrosis factor-␣ WORLDWIDE, 1

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Section: Discussionmentioning

confidence: 99%

Detrimental metabolic effects of combining long-term cigarette smoke exposure and high-fat diet in mice

Chen¹,

Hansen²,

Jones³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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“…In previous studies, we [18] and others [33] demonstrated that glucose excites AP neurons that to a large proportion are activated by amylin. Furthermore, hypoglycaemic plasma glucose levels, ranging between 1.6 and 2.2 m M , have been shown to prevent amylin from inhibiting both gastric emptying and glucagon secretion [34, 35].…”

Section: Discussionmentioning

confidence: 99%

Diet-Derived Nutrients Modulate the Effects of Amylin on c-Fos Expression in the Area Postrema and on Food Intake

et al. 2007

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The pancreatic hormone amylin decreases food intake via activation of area postrema (AP) neurons. We investigated whether amylin’s potency to reduce food intake and to induce c-Fos expression in the AP/nucleus of the solitary tract region is affected by the feeding conditions and specifically by the macronutrient composition of the diet. Whereas a low dose of amylin (5 µg/kg s.c.) induced very little c-Fos expression in ad libitum chow fed rats, it caused a strong c-Fos expression in 24-hour food-deprived rats and in rats that received a nutrient-deficient non-caloric mash (NCM; vanilla-flavoured cellulose) 24 h before injection. To reveal the contribution of single nutrients to the low c-Fos expression after chow feeding, amylin-induced c-Fos was analyzed after feeding NCM that was selectively supplemented with glucose, fat (lard), or protein (casein), matching the intake of these nutrients of chow-fed rats. While the rats fed NCM supplemented with glucose or fat displayed an equally strong amylin-induced activation as fasted rats or rats fed plain NCM, a significantly lower c-Fos expression was observed in rats fed a protein-supplemented NCM or a NCM containing all three nutrients. In line with this lower activation, the same dose of amylin failed to reduce food intake in NCM/protein-fed rats, while amylin caused a reduction in feeding when animals received NCM, NCM/glucose, or NCM/fat. Interestingly, amylin effectively reduced food intake in ad libitum chow fed rats despite the low level of amylin-induced c-Fos expression in the AP under these conditions. We conclude that the anorectic potential of amylin may be attenuated by diet-derived proteins, whereas this effect appears to be overridden when the amount of carbohydrates/fat is high relative to the protein content, such as, e.g., in standard chow.

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“…This issue is of particular interest because amylinsensitive neurons have been shown to be glucose-responsive [26,27]. Furthermore, amylin's inhibition of gastric emptying, which also depends on the AP, is overridden by hypoglycemia [28].…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

Amylin and GLP-1 target different populations of area postrema neurons that are both modulated by nutrient stimuli

Züger¹,

K²,

Lutz³

et al. 2013

Physiology & Behavior

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(2013). Amylin and GLP-1 target different populations of area postrema neurons that are both modulated by nutrient stimuli. Physiology and Behavior,[112][113] This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPTThe area postrema mediates the hypophagic effect of the pancreatic hormone amylin and is also sensitive to glucagon-like peptide 1 (GLP-1). Protein seems to modulate amylin responsiveness because amylin seems to produce a stronger hypophagic effect and a stronger c-Fos expression when protein is absent from the diet. Accordingly, amylin induces a stronger c-Fos expression in the AP when injected in fasted compared to ad libitum fed rats.Here we tested the hypothesis that diet-derived protein attenuates the amylin dependent suppression of feeding and AP activation using isocaloric diets that differed in their protein content. Moreover, we investigated whether peripheral amino acid injection attenuates amylin-induced c-Fos expression in fasted rats. Since recent evidence suggests that GLP-1 may also reduce eating via the AP we tested whether 24h fasting also increases neuronal AP responsiveness to GLP-1 similar to the fasting-induced increase in amylin responsiveness. A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPT 2In conclusion, our findings support a protein-dependent modulation of behavioral and neuronal amylin responsiveness under equicaloric feeding conditions. Amino acids might contribute to the inhibitory effect of diet-derived protein to reduce amylin-induced neuronal AP activation. Neuronal AP responsiveness to GLP-1 is also increased in the fasted state suggesting that diet-derived nutrients may also interfere with AP-mediated GLP-1 effects.Nevertheless, the primary target neurons for amylin appear to be distinct from cells targeted by GLP-1 and by stimuli producing aversion (LiCl) or contributing to blood pressure regulation (AngII) via the AP. Since amylin and GLP-1 analogs are targets for the treatment of obesity, the nutrient-dependent modulation of AP responsiveness might entail implications for such therapeutic approaches.

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Glucose‐Responsive Neurons In the Brainstem

Cited by 83 publications

References 13 publications

Detrimental metabolic effects of combining long-term cigarette smoke exposure and high-fat diet in mice

Detrimental metabolic effects of combining long-term cigarette smoke exposure and high-fat diet in mice

Diet-Derived Nutrients Modulate the Effects of Amylin on c-Fos Expression in the Area Postrema and on Food Intake

Amylin and GLP-1 target different populations of area postrema neurons that are both modulated by nutrient stimuli

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