Visceral factors in the control of food intake

Stricker, Edward M.; McCann, Michael T.

doi:10.1016/0361-9230(85)90119-4

Cited by 18 publications

(6 citation statements)

References 44 publications

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“…vagal and spinal. Since the vagal afferents have been implicated in feeding behavior [107], spinal and vagal afferents may serve opposing functions analogous to those proposed for the glucose-excited and glucose-inhibited neurons of the CNS [64]. …”

Section: ) Distributed Network Of Glucosensorsmentioning

confidence: 99%

Sweet talk in the brain: Glucosensing, neural networks, and hypoglycemic counterregulation

Watts¹,

Donovan²

2010

Frontiers in Neuroendocrinology

148

138

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Glucose is the primary fuel for the vast majority of cells, and animals have evolved essential cellular, autonomic, endocrine, and behavioral measures to counteract both hypo-and hyperglycemia. A central component of these counterregulatory mechanisms is the ability of specific sensory elements to detect changes in blood glucose and then use that information to produce appropriate counterregulatory responses. Here we focus on the organization of the neural systems that are engaged by glucosensing mechanisms when blood glucose concentrations fall to levels that pose a physiological threat. We employ a classic sensori-motor integrative schema to describe the peripheral, hindbrain, and hypothalamic components that make up counterregulatory mechanisms in the brain. We propose that models previously developed to describe how the forebrain modulates autonomic reflex loops in the hindbrain offer a reasoned framework for explaining how counterregulatory neural mechanisms in the hypothalamus and hindbrain are structured.

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Section: ) Distributed Network Of Glucosensorsmentioning

confidence: 99%

Sweet talk in the brain: Glucosensing, neural networks, and hypoglycemic counterregulation

Watts¹,

Donovan²

2010

Frontiers in Neuroendocrinology

148

138

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“…8 Under physiologic conditions, the stomach empties food into the small intestine in a fine-tuned way, mainly depending on the calorie load of the stomach. 38 Gastric emptying is regulated by afferent nerve fibers and CCK, 39 resulting in the release of food into the small intestine adapted to the absorptive capacity of the small intestine. 38 After total gastrectomy, food enters the upper small intestine immediately, where it activates signal pathways to the brain that initiate satiation and inhibit food intake.…”

Section: Regulation Of Food Intake After Total Gastrectomy In Ratsmentioning

confidence: 99%

“…38 Gastric emptying is regulated by afferent nerve fibers and CCK, 39 resulting in the release of food into the small intestine adapted to the absorptive capacity of the small intestine. 38 After total gastrectomy, food enters the upper small intestine immediately, where it activates signal pathways to the brain that initiate satiation and inhibit food intake. For example, CCK is released prematurely and at a greater rate after gastrectomy, 10,17 while the inhibitory effects on food intake are preserved after total gastrectomy.…”

Section: Regulation Of Food Intake After Total Gastrectomy In Ratsmentioning

confidence: 99%

Total Gastrectomy Severely Alters the Central Regulation of Food Intake in Rats

Zittel¹,

Glatzle²,

Müller³

et al. 2002

Annals of Surgery

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ObjectiveTo investigate the central regulation of food intake by quantifying neuron activation of the nucleus of the solitary tract (NTS) after injection of cholecystokinin (CCK) or food intake in gastrectomized rats. Summary Background DataTotal gastrectomy is followed by early satiety, low calorie intake, and weight loss in the majority of patients. The etiology of these effects is unknown. Sixty percent to 70% of patients remain underweight after total gastrectomy, the weight loss averaging 25% of preoperative body weight. About two thirds of gastrectomized patients report early satiety, and about 60% do not reach the recommended daily calorie intake. The NTS is a brain stem center involved in the regulation of food intake; thus, the extent and pattern of neuronal activation provide information on the process involved in the initiation of satiation and the regulation of food intake. MethodsThe authors investigated neuronal activation in the NTS using c-fos immunohistochemistry following CCK injection or food intake in healthy control rats, sham-operated control rats, age-matched control rats, weight-matched control rats, and vagotomized or gastrectomized rats. ResultsNeuronal activation in the NTS after CCK injection was significantly decreased 21 days after total gastrectomy, but increased by up to 51% 3 months and by up to 102% 12 months after surgery compared to age-matched unoperated control rats. Neuronal activation in the NTS in response to feeding was markedly increased up to fivefold in gastrectomized rats. This increase was early in onset and sustained, and occurred despite significantly reduced food intake. Administration of MK329, a CCK-A receptor antagonist, significantly reduced the number of postprandially activated neurons in both gastrectomized and control rats. ConclusionsThe early postprandial activation of NTS neurons after total gastrectomy in rats may correspond to early satiety reported by patients, while the sustained activation of NTS neurons after a meal could contribute to a reduced daily calorie intake. These data suggest that a disturbed central regulation of food intake might contribute to early satiety, reduced food intake, and weight loss after total gastrectomy.Total gastrectomy is still a mainstay of gastric cancer treatment.1 It is followed by a variety of symptoms and impairments, commonly referred to as postgastrectomy syndromes.2 One important feature of the postgastrectomy syndromes is a considerable loss of body weight.3,4 The loss averages around 25% of preoperative body weight 4,5 and leaves 60% to 70% of patients permanently below ideal body weight. 3,6 While perioperative weight loss due to catabolic metabolism is generally followed by an anabolic phase 3 to 8 days postoperatively with body weight recovery, 7 this is not the case in gastrectomized patients, where weight loss and underweight frequently cause long-lasting morbidity. 4 -6,8 There is evidence that pancreatic insufficiency, resulting in malabsorption and impaired food utilization, contributes Correspon...

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“…Interestingly, McHugh & Moran (1985) found that delivery of energy directly to the intestines decreased food intake and slowed gastric emptying. In contrast, in rats (Stricker & McCann, 1985) as well as in man (Schvarcz et al 1993), insulin produced a marked increase in gastric emptying. Gastric emptying rate was studied in patients with type I diabetes mellitus submitted to an insulinglucose clamp.…”

mentioning

confidence: 72%

“…How are the rate of absorption, the rate of glucose disposal and the decline in blood glucose related? Stricker & McCann (1985) reported that, in the rat, after an initial bolus, gastric loads of concentrated glucose solutions emptied at a relatively constant rate (126-188 J/min) approximately equal to the BMR. The gastric emptying rate of normal-sized chow meals offered to rats after a minimal food deprivation was also found to be approximately 188 J/min and constant for most of the emptying period (Newman & Booth, 1981) with, however, a slowing near the end.…”

mentioning

confidence: 99%

Glucose utilization dynamics and food intake

Louis-Sylvestre

1999

Br J Nutr

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Visceral factors in the control of food intake

Cited by 18 publications

References 44 publications

Sweet talk in the brain: Glucosensing, neural networks, and hypoglycemic counterregulation

Sweet talk in the brain: Glucosensing, neural networks, and hypoglycemic counterregulation

Total Gastrectomy Severely Alters the Central Regulation of Food Intake in Rats

Glucose utilization dynamics and food intake

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