Gastric distension induces c-Fos in medullary GLP-1/2-containing neurons

Vrang, Niels; Phifer, Curtis B.; Corkern, Michele; Berthoud, Hans‐Rudolf

doi:10.1152/ajpregu.00732.2002

Cited by 188 publications

(164 citation statements)

References 46 publications

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“…Furthermore, in rats GLP-1-producing neurons are activated by distension of the stomach and enteroceptive stress [27,28]. This could indicate a neuronal transmission of satiety signals from the gastrointestinal tract into the brain through the "brain GLP-1 system".…”

Section: Glucagon-like Peptide-1 (Glp-1) Physiologymentioning

confidence: 99%

Therapy for Obesity Based on Gastrointestinal Hormones

Christensen¹,

Knop²,

Vilsbøll³

2011

Rev Diabet Stud

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■ AbstractIt has long been known that peptide hormones from the gastrointestinal tract have significant impact on the regulation of nutrient metabolism. Among these hormones, incretins have been found to increase insulin secretion, and thus incretin-based therapies have emerged as new modalities for the treatment of type 2 diabetes. In contrast to other antidiabetic treatments, these agents have a positive outcome profile on body weight. Worldwide there are 500 million obese people, and 3 million are dying every year from obesityrelated diseases. Recently, incretin-based therapy was proposed for the treatment of obesity. Currently two different incretin therapies are widely used in the treatment of type 2 diabetes: 1) the GLP-1 receptor agonists which cause significant and sustained weight loss in overweight patients, and 2) dipeptidyl peptidase 4 (DPP-4) inhibitors being weight neutral. These findings have led to a greater interest in the physiology of intestinal peptides with potential weightreducing properties. This review discusses the effects of the incretin-based therapies in obesity, and provides an overview of intestinal peptides with promising effects as potential new treatments for obesity.

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Section: Glucagon-like Peptide-1 (Glp-1) Physiologymentioning

confidence: 99%

Therapy for Obesity Based on Gastrointestinal Hormones

Christensen¹,

Knop²,

Vilsbøll³

2011

Rev Diabet Stud

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“…We were struck by this expression pattern, as medial NTS neurons were also known to process GI vagal afferent signals arising from ingesta interacting with the stomach and intestine, [54][55][56][57][58][59] and set out to address whether leptin signaling (intraperitoneal leptin-induced pSTAT3-IR) and physiological levels of gastric distension-induced Fos-IR were expressed by the same NTS neurons. We found that B40% of pSTAT3-IR medial NTS neurons are also responsive to gastric distention.…”

Section: Glp-1mentioning

confidence: 99%

The nucleus tractus solitarius: a portal for visceral afferent signal processing, energy status assessment and integration of their combined effects on food intake

2009

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For humans and animal models alike there is general agreement that the central nervous system processing of gastrointestinal (GI) signals arising from ingested food provides the principal determinant of the size of meals and their frequency. Despite this, relatively few studies are aimed at delineating the brain circuits, neurochemical pathways and intracellular signals that mediate GI-stimulation-induced intake inhibition. Two additional motivations to pursue these circuits and signals have recently arisen. First, the success of gastric-bypass surgery in obesity treatment is highlighting roles for GI signals such as glucagon-like peptide-1 (GLP-1) in intake and energy balance control. Second, accumulating data suggest that the intakereducing effects of leptin may be mediated through an amplification of the intake-inhibitory effects of GI signals. Experiments reviewed show that: (1) the intake-suppressive effects of a peripherally administered GLP-1 receptor agonist is mediated by caudal brainstem neurons and that forebrain-hypothalamic neural processing is not necessary for this effect; (2) a population of medial nucleus tractus solitarius (NTS) neurons that are responsive to gastric distention is also driven by leptin; (3) caudal brainstem-targeted leptin amplifies the food-intake-inhibitory effects of gastric distention and intestinal nutrient stimulation; (4) adenosine monophosphate-activated protein kinase (AMPK) activity in NTS-enriched brain lysates is elevated by food deprivation and reduced by refeeding and (5) the intake-suppressive effect of hindbrain-directed leptin is reversed by elevating hindbrain AMPK activity. Overall, data support the view that the NTS and circuits within the hindbrain mediate the intake inhibition of GI signals, and that the effects of leptin on food intake result from the amplification of GI signal processing.

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“…The NTS receives a broad spectrum of sensory signals from the gut, carried in part by the subdiaphragmatic vagus nerve; signals include sensory input from liver, stomach, and intestinal receptors (Powley, 2000;Saper et al, 2002;Vrang et al, 2003). These signals may be associated with the homeostatic control of feeding, and possibly involved in initiation or termination of meals (Saper et al, 2002).…”

Section: Functional Considerationsmentioning

confidence: 99%