Chronic ICV Enterostatin Preferentially Reduced Fat Intake and Lowered Body Weight

Lin, Lih-Yuan; Chen, J.; York, David A.

doi:10.1016/s0196-9781(97)00128-9

Cited by 58 publications

(44 citation statements)

References 29 publications

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“…However, as the 'ileal-brake' has been shown to be dosedependent (Pironi et al, 1993), this is compatible with the present results, given that when dose levels of Olibra TM fat increased, energy and macronutrient intakes were further lowered. Thus, it may be that Olibra TM is acting through an increased and prolonged release of peptides such as peptide YY (Pironi et al, 1993), cholecystokinin (Lieverse et al, 1994;Smith & Gibbs, 1994), glucagon-like peptide-1 (Naslund et al, 1998;Giralt & Vergara, 1999), or enterostatin (ErlansonAlbertson & York, 1997;Lin et al, 1997) which are known to influence satiety through the 'ileal-brake'.…”

Section: Discussionmentioning

confidence: 99%

Dose–response effects of a novel fat emulsion (Olibra™) on energy and macronutrient intakes up to 36 h post-consumption

et al. 2002

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Objective: To investigate the dose -response effects of a novel fat emulsion (Olibra TM ) on energy and macronutrient intakes up to 36 h post-consumption in non-overweight subjects. Design: A single-blind, placebo-controlled, within-subject cross-over design was used. Setting: Metabolic suite of the University of Ulster, Coleraine. Subjects: Fifty subjects (30 female, 20 male) from the student and staff population of the University of Ulster, Coleraine. Interventions: Subjects were given in random order, 7 days apart, a 200 g portion of yoghurt containing a total of 15 g of fat, which varied in quantity of Olibra TM fat (0, 2, 4, 6 g) at 09:00 h. At 13:00 h subjects were given ad libitum access to a range of foods. Amounts of food consumed were measured by covert pre-and post-consumption weighing of individual serving dishes. For the remainder of the day and the following 24 h, subjects weighed and recorded all food intakes. 39.3, 38.2, 39.6% energy), intakes were progressively reduced with increasing doses of Olibra TM fat in the total group (P < 0.001). A similar response was observed in the female group up to 4 g (P < 0.001) and in the male group after 2 and 6 g (P < 0.05). Energy and macronutrient intakes for the remainder of each study day and over the following 24 h were significantly lower after all dose levels compared to the control (P < 0.001). Conclusion:The results suggest that Olibra TM fat reduced the effect of overeating during an ad libitum lunch meal and subsequent food intake up to 36 h post-consumption.

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Section: Discussionmentioning

confidence: 99%

Dose–response effects of a novel fat emulsion (Olibra™) on energy and macronutrient intakes up to 36 h post-consumption

et al. 2002

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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).It has been hypothesized that the role of the amygdala in the overall complex feeding behavior is to mediate responses that modulate the behavior. Multiple laboratories have investigated the role of the amygdala on different aspects of the feeding behavior, including the role in food reward (4,18,20,25) and food aversion (43, 54).…”

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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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“…However, we have shown that chronic administration of enterostatin is associated with weight loss and reduction in adipose mass that appears to be only partly related to the reduction in food intake. 34,35 It is possible that an antiangiogenic effect of enterostatin may contribute to an enterostatin-induced loss of body weight by promoting adipose tissue loss and increasing the availability of fatty acids for oxidation. To date we have only shown the antiangiogenic effect of enterostatin in vitro in culture systems.…”

Section: Discussionmentioning

confidence: 99%

Enterostatin inhibition of angiogenesis: possible role of pAMPK and vascular endothelial growth factor A (VEGF-A)

Park

Lyons

et al. 2008

Int J Obes

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Introduction:We utilized a genomic analysis of the response of neuronal GT1-7 cells to enterostatin to identify pathways responsive to this peptide. This information, together with reported properties of the enterostatin receptor, suggested that enterostatin may have an effect on angiogenesis. Method: To investigate this hypothesis, we studied the effect of enterostatin as an antiangiogenic agent in two angiogenic tissue culture model systems.Results: Enterostatin induced a 50% or greater inhibition in the angiogenic response of human fat cells and had a U-shaped bimodal dose-response effect in inhibiting angiogenesis in a human placental vein angiogenesis model. To further understand this response, we tested enterostatin's effect in a human hepatoma cell line (HepG2 cells) that was subjected to glucose deprivation, a condition known to induce angiogenesis in other tumor cell lines. Phosphorylated AMP kinase (pAMPK) levels and vascular endothelial growth factor A (VEGF-A) mRNA expression were elevated robustly after incubation of HepG2 cells in the absence of glucose for 4 h, but 15 min incubation with enterostatin dramatically inhibited this pAMPK activation and reduced VEGF-A gene expression after 1 h incubation with enterostatin. The AMPK activator 5-aminoimidazole-4-carboximide ribonucleoside (AICAR) induced VEGF-A expression. Summary: These data suggest that enterostatin has an antiangiogenic effect and suggest that it regulates VEGF-A gene expression through inhibition of AMPK activity.

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Chronic ICV Enterostatin Preferentially Reduced Fat Intake and Lowered Body Weight

Cited by 58 publications

References 29 publications

Dose–response effects of a novel fat emulsion (Olibra™) on energy and macronutrient intakes up to 36 h post-consumption

Dose–response effects of a novel fat emulsion (Olibra™) on energy and macronutrient intakes up to 36 h post-consumption

Melanocortin activity in the amygdala controls appetite for dietary fat

Enterostatin inhibition of angiogenesis: possible role of pAMPK and vascular endothelial growth factor A (VEGF-A)

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