Food intake regulation in the weanling rat: effects of the most limiting essential amino acids of gluten, casein, and zein on the self-selection of protein and energy.
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The effects of altering the quality of the dietary protein source on the self-selection of protein and energy by the weanling rat simultaneously offered a choice of two diets differing only in protein concentration were tested. The protein-energy selected was measured when the first limiting amino acid lysine was added to gluten; when lysine, methionine, or the first four limiting amino acids were added to gluten or to casein; or when the nutritional quality of zein was altered by manipulation of the content of tryptophan, lysine, or the four most limiting amino acids. The additions of lysine to gluten caused a decrease in the protein-energy selected and an increase in growth rate of the weanling rat. However, improving the amino acid balance of casein or zein did not have this effect. It was concluded that the selection of protein and energy by weanling rats is not related to the nutritional quality of the protein fed. (+info)
Neuron-specific expression of human angiotensinogen in brain causes increased salt appetite.
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The brain renin-angiotensin system (RAS) has an important role in the regulation of cardiovascular function. In the brain, angiotensinogen (AGT) is expressed mainly in astrocytes (glia) and in some neurons in regions controlling cardiovascular activities. Because of the inability to dissect the functional role of astrocyte- vs. neuron-derived AGT in vivo by pharmacological approaches, the exact role of neuron-derived AGT in the regulation of blood pressure (BP) and fluid and electrolyte balance remains unclear. Therefore, we generated a transgenic mouse model overexpressing human AGT under the control of a neuron-specific (synapsin I) promoter (SYN-hAGT). These mice exhibited high-level expression of human AGT mRNA in the brain, with lower expression in the kidney and heart. Human AGT was not detected in plasma, but in the brain it was expressed exclusively in neurons. Intracerebroventricular (30 ng) but not intravenous (500 ng) injection of purified human renin (hREN) caused a pressor response, which was prevented by intracerebroventricular preinjection of the angiotensin II type 1 receptor antagonist losartan, indicating an AT(1) receptor-dependent functional role of neuron-derived AGT in the regulation of BP in response to exogenous REN. Double transgenic mice expressing both the hREN gene and SYN-hAGT transgene exhibited normal BP and water intake but had an increased preference for salt. These data suggest that neuronal AGT may play an important role in regulating salt intake and salt appetite. (+info)
Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery.
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BACKGROUND: Weight loss causes changes in appetite and energy expenditure that promote weight regain. Ghrelin is a hormone that increases food intake in rodents and humans. If circulating ghrelin participates in the adaptive response to weight loss, its levels should rise with dieting. Because ghrelin is produced primarily by the stomach, weight loss after gastric bypass surgery may be accompanied by impaired ghrelin secretion. METHODS: We determined the 24-hour plasma ghrelin profiles, body composition, insulin levels, leptin levels, and insulin sensitivity in 13 obese subjects before and after a six-month dietary program for weight loss. The 24-hour ghrelin profiles were also determined in 5 subjects who had lost weight after gastric bypass and 10 normal-weight controls; 5 of the 13 obese subjects who participated in the dietary program were matched to the subjects in the gastric-bypass group and served as obese controls. RESULTS: Plasma ghrelin levels rose sharply shortly before and fell shortly after every meal. A diet-induced weight loss of 17 percent of initial body weight was associated with a 24 percent increase in the area under the curve for the 24-hour ghrelin profile (P=0.006). In contrast, despite a 36 percent weight loss after gastric bypass, the area under the curve for the ghrelin profile in the gastric-bypass group was 77 percent lower than in normal-weight controls (P<0.001) and 72 percent lower than in matched obese controls (P=0.01). The normal, meal-related fluctuations and diurnal rhythm of the ghrelin level were absent after gastric bypass. CONCLUSIONS: The increase in the plasma ghrelin level with diet-induced weight loss is consistent with the hypothesis that ghrelin has a role in the long-term regulation of body weight. Gastric bypass is associated with markedly suppressed ghrelin levels, possibly contributing to the weight-reducing effect of the procedure. (+info)
The effect of guar gum addition to a semisolid meal on appetite related to blood glucose, in dieting men.
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OBJECTIVE: To investigate whether addition of modified guar gum (GG) to a low-energy semisolid meal might be effective on appetite by modifying the response of blood glucose and other blood parameters. DESIGN: Three intervention periods of 2 weeks each, separated by washout periods of 4 weeks. Randomized and cross-over design. SUBJECTS: Fifteen overweight male subjects (mean+/-s.d.; age, 44+/-9 y; body mass index, 28.6+/-1.8 kg/m(2)). INTERVENTION: Subjects consumed a low-energy diet divided over three times a day, consisting of a semisolid meal with (SSM+) or without (SSM) addition of 2.5 g GG, or a solid meal (SM) with the same energy content (947 kJ) and macronutrient composition, plus a dinner of the subject's own choice. At the end of each intervention, time and number of meal initiations, dynamics of blood glucose and other blood parameters, and appetite ratings such as hunger and satiety were determined in a time-blinded situation. RESULTS: The changes in blood glucose from meal initiation to blood glucose peak and from peak to nadir were smaller with SSM+ and SM compared to SSM. Satiety before the third meal was higher with SSM+ and SM compared to SSM (P<0.01). Meal pattern, general appetite and total energy intake were similar for all treatments. CONCLUSIONS: We conclude that, similar to SM, SSM+ resulted in a more moderate change in blood glucose compared to SSM and positively affected satiety before the third meal, while general appetite, total energy intake and meal pattern did not differ. (+info)
Total gastrectomy severely alters the central regulation of food intake in rats.
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OBJECTIVE: To 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 DATA: Total 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. METHODS: The 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. RESULTS: Neuronal 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. CONCLUSIONS: The 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. (+info)
Stomach and upper intestine of the rat in the regulation of food intake.
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The role of the upper intestine in the regulation of food intake and gastric emptying has been studied in normal, gastrectomized, and "crossover" rats, parabiotic rats with a common visceral cavity in which the proximal duodenum of each parabiont is anastomosed to the pylorus of the stomach of the partner. One rat of "crossover" pairs eats and the partner eats little or nothing. Normal rats fed a raw soybean (RS) diet ate less and gastric evacuation proceeded more slowly than in normal rats fed a heated soybean (HS) diet. It is postulated that RS contains a heat-labile intestinal irritant. The upper intestine of gastrectomized rats regulates food intake and prevents overloading of the intestine. Force feeding of excessive amounts of the RS diet elicited the secretion of much more solids and nitrogen into the upper intestine than did similar amounts of the HS diet. The upper intestines of "crossover" rats lose all control over entry of gastric contents into their duodena. Fed ad libitum, the parabiont whose stomach emptied first, ate continuously, while the recipient partner showed diarrhea. It is postulated that the control of food intake traditionally assigned to the stomach resides, rather, in the upper intestine. (+info)
A peripheral mechanism for CB1 cannabinoid receptor-dependent modulation of feeding.
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Recent studies suggest that the endocannabinoid system modulates feeding. Despite the existence of central mechanisms for the regulation of food intake by endocannabinoids, evidence indicates that peripheral mechanisms may also exist. To test this hypothesis, we investigated (1) the effects of feeding on intestinal anandamide accumulation; (2) the effects of central (intracerebroventricular) and peripheral (intraperitoneal) administration of the endocannabinoid agonist anandamide, the synthetic cannabinoid agonist R-(+)-(2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrol[1,2,3-de]-1,4-benzoxaz in-6-yl)(1-naphthalenyl) methanone monomethanesulfonate (WIN55,212-2), and the CB1-selective antagonist N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3-carboxa mide (SR141716A) on food intake in rats; and (3) the effects of sensory deafferentation on the modulation of feeding by cannabinoids. Food deprivation produced a sevenfold increase in anandamide content in the small intestine but not in the brain or stomach. Refeeding normalized intestinal anandamide levels. Peripheral but not central administration of anandamide or WIN55,212-2 promoted hyperphagia in partially satiated rats. Similarly, peripheral but not central administration of SR141716A reduced food intake. Capsaicin deafferentation abolished the peripheral effects of both cannabinoid agonists and antagonists, suggesting that these agents modulate food intake by acting on CB1 receptors located on capsaicin-sensitive sensory terminals. Oleoylethanolamide, a noncannabinoid fatty ethanolamide that acts peripherally, prevented hyperphagia induced by the endogenous cannabinoid anandamide. Pretreatment with SR141716A enhanced the inhibition of feeding induced by intraperitoneal administration of oleoylethanolamide. The results reveal an unexpected role for peripheral CB1 receptors in the regulation of feeding. (+info)
Nicotinic receptor-mediated effects on appetite and food intake.
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It is well known, although not well understood, that smoking and eating just do not go together. Smoking is associated with decreased food intake and lower body weight. Nicotine, administered either by smoking or by smokeless routes, is considered the major appetite-suppressing component of tobacco. Perhaps the most renowned example of nicotine's influence on appetite and feeding behavior is the significant weight gain associated with smoking cessation. This article presents an overview of the literature at, or near, the interface of nicotinic receptors and appetite regulation. We first consider some of the possible sites of nicotine's action along the complex network of neural and non-neural regulators of feeding. We then present the hypothesis that the lateral hypothalamus is a particularly important locus of the anorectic effects of nicotine. Finally, we discuss the potential role of endogenous cholinergic systems in motivational feeding, focusing on cholinergic pathways in the lateral hypothalamus. (+info)