Differential Effects of Baseline Macronutrient Preferences on Macronutrient Selection After Galanin, NPY, and an Overnight Fast

Smith, Brenda K.; Berthoud, Hans‐Rudolf; York, David A.; Bray, George A.

doi:10.1016/s0196-9781(96)00318-x

Cited by 75 publications

(65 citation statements)

References 12 publications

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“…The role of other peptides is less clear. Although galanin has been linked to fat intake in some studies (34), its effects are strongly influenced by background preferences such that it selectively stimulates carbohydrate in carbohydrate-preferring rats (67). Likewise, serotonin was initially linked to carbohydrate feeding (86), but more recent evidence suggests that serotonin agonists selectively inhibit fat intake (5,68).…”

Section: Introductionmentioning

confidence: 99%

Enterostatin‐A Peptide Regulating Fat Intake

Erlanson–Albertsson

York

1997

Obesity Research

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YORK. Enterostatin-a peptide regulating fat intake. Obes Res. 1997;5:360-372. A high fat intake, together with an inability to match lipid oxidation to fat intake, has been found to be correlated with obesity in humans. This review describes our current understanding of enterostatin, a peptide that selectively reduces fat intake. Enterostatin is formed in the intestine by the cleavage of secreted pancreatic procolipase, the remaining colipase serving as an obligatory cofactor for pancreatic lipase during fat digestion. Enterostatin is also produced in the gastric mucosa and the mucosal epithelia of the small intestine. Procolipase gene transcription and enterostatin release into the gastrointestinal lumen are increased by high-fat diets. After feeding, enterostatin appears in the lymph and circulation. Enterostatin will selectively inhibit fat intake during normal feeding and in experimental paradigms that involve dietary choice. Its anorectic effect has been demonstrated in a number of species. Both peripheral and central sites of action have been proposed. The peripheral mechanism involves an afferent vagal signaling pathway to hypothalamic centers. The central responses are mediated through a pathway that includes both serotonergic and opioidergic components. Chronically, enterostatin reduces fat intake, bodyweight, and body fat. This response may involve multiple metabolic effects of enterostatin, which include a reduction of insulin secretion, an increase in sympathetic drive to brown adipose tissue, and the stimulation of adrenal corticosteroid secretion. A possible pathophysiological role is suggested by studies that have linked low enterostatin production andor responsiveness to strains of rat that become obese and prefer dietary fat. Humans with obesity also exhibit a lower secretion of pancreatic procolipase after a test meal, compared with persons of normal weight.

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Section: Introductionmentioning

confidence: 99%

Enterostatin‐A Peptide Regulating Fat Intake

Erlanson–Albertsson

York

1997

Obesity Research

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“…For example, the orexigenic NPY (47,48,50) , norepinephrine (30,50), or agouti-related protein (AgRP) (23) have been reported to induce specific selection of macronutrients. Enterostatin, a satiety factor secreted in the gastrointestinal tract and expressed also in the central nervous system, induces an immediate reduction in food intake and inhibits appetite specifically for dietary fat when injected peripherally or centrally (31,37,39).…”

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confidence: 99%

Melanocortin activity in the amygdala controls appetite for dietary fat

Boghossian

Park

York

2010

American Journal of Physiology-Regulatory, Integrative and Comp

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The amygdala is rich in melanocortin 4 receptors. Because the reduction in dietary fat intake after enterostatin is injected in the central nucleus of the amygdala (CeA) is blocked by a melanocortin 4 receptor antagonist, we investigated the role of melanocortin activity in the CeA in regulating food intake and macronutrient choice. Sprague-Dawley rats, fitted with CeA cannulas, were fed either chow, a high-fat (HF) diet, or adapted to a two-choice HF or low-fat (LF) diet. Injections of the MC4R agonist melanotan II (MTII) in the CeA had a dose-dependent inhibitory effect on food intake that lasted for at least 24 h. This response was greater in rats fed a HF diet. The inverse agonist agouti-related protein (AgRP) and antagonist SHU-9119 increased food intake in a dose-dependent manner, with the hyperphagia lasting for 60 h. In rats adapted to a two-choice HF/LF diet, MTII decreased HF consumption but had no effect on LF consumption, resulting in a long-lasting decrease in total calorie intake (Ϫ35.5% after 24 h, P Ͻ 0.05). Total calorie intake increased in both AgRP-and SHU-9119-treated rats (32 and 109% after 24 h, respectively) as the result of increased intake of HF diet. There was no modification of LF consumption with AgRP treatment and a transient nonsignificant decrease with SHU-9119 treatment. Amygdala brain-derived neurotrophic factor expression was increased by AgRP in fed rats. These results identify the amygdala as a site of action for the melanocortin system to control food intake and dietary preferences.agouti-related protein; melanotan II; SHU-9119; brain derived neurotrophic factor, food intake FOR YEARS, HYPOTHALAMIC CENTERS have been considered as the major brain centers regulating food intake and/or macronutrient selection (45). The neural circuits involved in the regulation of feeding behavior are complex, and more recent studies implicate other parts of the brain in the regulation of ingestive behaviors. Areas such as the nucleus accumbens, the amygdala, the brain stem, and many others form together with the hypothalamic areas a complex circuitry regulating all levels of feeding behavior (6,8,55). Indeed, the paraventricular nucleus (PVN) is not essential for either neuropeptide Y (NPY)-induced feeding or the anorexic response to melanocortin activity (16) since both are evident in PVN-lesioned rats. Furthermore, the anorectic response to melanotan II (MTII) is evident in the dorsovagal complex of the brain stem (52,58).A number of neuropeptides and compounds are known to selectively affect macronutrient intake when administered centrally. For example, the orexigenic NPY (47, 48, 50) , norepinephrine (30, 50), or agouti-related protein (AgRP) (23) have been reported to induce specific selection of macronutrients. Enterostatin, a satiety factor secreted in the gastrointestinal tract and expressed also in the central nervous system, induces an immediate reduction in food intake and inhibits appetite specifically for dietary fat when injected peripherally or centrally (31,37,39).It has been hy...

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“…It has been reported that baseline macronutrient preferences are an important consideration in studies examining the effects of pharmacological or physiological treatments on macronutrient selection (3,13,24,25). The present study was designed to qualify the neuromodulatory effects of GAL and 5 -HT on macronutrient intake in self-selecting rats with macronutrient preferences.…”

Section: Discussionmentioning

confidence: 99%

“…Macronutrient preferences were characterized based on the ratio of fat intake to carbohydrate intake, e.g., carbohydrate-preferring rats were those whose fat to carbohydrate ratio was less than 1, and fat-preferring rats were those whose fat to carbohydrate ratio was greater than 1 (25). We also used these categories to divide rats into two groups by macronutrient preferences.…”

Section: Discussionmentioning

confidence: 99%

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Serotonergic regulation of galanin-induced selective macronutrient intake in self-selecting rats

Tanaka

Kido

2008

J. Med. Invest.

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: We investigated macronutrient intake after intraventricular injection of galanin (GAL, 3 nmol/5 μl/rat) and/or serotonin (5-HT, 50 nmol/5 μl/rat) in self-selecting fasted rats with preferences for either carbohydrates or fats. GAL injection significantly increased carbohydrate and total intake in all rats irrespective of macronutrient preference, whereas 5-HT alone did not affect macronutrient intake. The GAL-induced increase in total intake decreased to the level of saline controls when GAL was coinjected with 5-HT. The ratio of kilocalories of carbohydrates, fats and proteins (macronutrient energy ratio) after injections of GAL and/or 5-HT was similar to the saline control. In carbohydrate-preferring rats, GAL increased carbohydrate, protein and fat intake as well as total intake. Coinjection of GAL and 5-HT tended to decrease carbohydrate intake, but increase protein and fat intake. The macronutrient energy ratio after injection of GAL did not change, but the carbohydrate energy ratio decreased after 5-HT was injected, with or without GAL. In contrast, in fat-preferring rats, GAL significantly increased carbohydrate intake. Injection of 5-HT with or without GAL did not change total macronutrient intake. The macronutrient energy ratio did not change after GAL injection with or without 5-HT. These differences suggest that macronutrient preferences should be considered in any macronutrient intake study, and that serotonergic neurons play a part in the regulation of GAL-induced macronutrient intake.

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Differential Effects of Baseline Macronutrient Preferences on Macronutrient Selection After Galanin, NPY, and an Overnight Fast

Cited by 75 publications

References 12 publications

Enterostatin‐A Peptide Regulating Fat Intake

Enterostatin‐A Peptide Regulating Fat Intake

Melanocortin activity in the amygdala controls appetite for dietary fat

Serotonergic regulation of galanin-induced selective macronutrient intake in self-selecting rats

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