Understanding the control of ingestive behavior in primates

Wilson, Mark; Moore, C.; Ethun, Kelly F.; Johnson, Zachary P.

doi:10.1016/j.yhbeh.2014.04.005

Cited by 10 publications

(5 citation statements)

References 206 publications

(225 reference statements)

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“…These findings are consistent with previous research findings that experimentally induced lower social status resulted in higher energy intake in humans and primates (33, 34). It has been previously shown that selection of high calorie food is predicted by perception of scarcity, and not taste (35).…”

Section: Discussionsupporting

confidence: 93%

Subjective social status is associated with compensation for large meals – A prospective pilot study

et al. 2019

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Section: Discussionsupporting

confidence: 93%

Subjective social status is associated with compensation for large meals – A prospective pilot study

et al. 2019

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“…In several cases, animals were shown to select unique combinations of different foods to obtain the same macronutrient intake (e.g. Chambers, Simpson, & Raubenheimer, 1995;Lee et al, 2008;Raubenheimer & Jones, 2006), proving that macronutrient intake targets are achieved through active homeostatic regulation involving neuronal and hormonal mechanisms (Schwartz & Zeltser, 2013;Wilson, Moore, Ethun, & Johnson, 2014).…”

Section: Introductionmentioning

confidence: 99%

Nutrient‐specific compensation for seasonal cold stress in a free‐ranging temperate colobine monkey

et al. 2018

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Homeostatic responses of animals to environmentally induced changes in nutrient requirements provide a powerful basis for predictive ecological models, and yet, such responses are virtually unstudied in the wild. We tested for macronutrient‐specific compensatory feeding responses by free‐ranging golden snub‐nosed monkeys (Rhinopithecus roxellana) inhabiting high altitude temperate forests, where they experience a substantial difference in ambient temperature in cold winters vs. warmer springs. The monkeys had free access to natural foods throughout the year, and to ensure that any seasonal differences in nutrient intake were due to homeostatic compensation and not constraints on food availability, we studied the monkeys during periods in which they were provisioned with the same amount of supplementary foods in winter and spring. Thermoregulatory energy costs in winter and spring were calculated using partitional calorimetric estimations of convective and radiative heat loss obtained from thermal imaging of free‐ranging monkeys in situ. Daily nutrient intakes were measured using continuous focal follows (average 6.9 hr/day) of free‐ranging individuals (27 days in spring and 28 days in winter). We used a nutritional geometry framework to integrate these data and test three predictions: (a) In order to remain thermoneutral (balance heat loss with heat expenditure), golden snub‐nosed monkeys increase daily energy consumption during the winter compared to spring; (b) this increase is achieved specifically by increasing intake of the primary energetic nutrients, carbohydrate and lipid, relative to protein; and (c) the seasonal increase in ingested fat and carbohydrate calories will quantitatively match the additional thermoregulatory costs in winter compared with spring. Our results showed that daily metabolisable energy intake in winter (721.5 kJ/mbm) was 1.8 times that in spring (399 kJ/mbm). As predicted, this difference was specific to fat and carbohydrate, whereas seasonal protein intake did not differ significantly. Winter consumption of fat and carbohydrate was 326 kJ/mbm per day greater than in spring, a value that closely matched the seasonal difference in the daily energetic costs of thermoregulation (329 kJ/mbm). This is the first study to test for a match between nutrient‐specific homeostatic compensation and environmentally induced perturbations in nutrient requirements in free‐ranging animals and underpins the potential for the homeostasis framework to provide predictive power to ecological models.

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“…We note that it is already known that the PHcausing anorexigens fenfluramine, aminorex, phentermine and fluoxetine increase 5-HT in the hypothalamus (101)(102)(103)(104)(105) and that fenfluramine blunted GH responsiveness to GHRH (105). Moreover, estrogens are themselves anorexigenic through effects at the level of the hypothalamus (106,107) showing that the central effects of anorexigens can be female-biased. Additionally, it is already known that PY-STAT5 signaling in the hypothalamus is involved in regulating appetite and sex-biased changes in body weight (74)(75)(76)(77) (Figure 1).…”

Section: Synthesis Of the Literature On Sex Bias Mediated By The Neurmentioning

confidence: 68%

Hypothesis: Neuroendocrine Mechanisms (Hypothalamus-Growth Hormone-STAT5 Axis) Contribute to Sex Bias in Pulmonary Hypertension

Sehgal

Yang

Miller

2015

Mol Med

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Pulmonary hypertension (PH) is a disease with high morbidity and mortality. The prevalence of idiopathic pulmonary arterial hypertension (IPAH) and hereditary pulmonary arterial hypertension (HPAH) is approximately two-to four-fold higher in women than in men. Paradoxically, there is an opposite male bias in typical rodent models of PH (chronic hypoxia or monocrotaline); in these models, administration of estrogenic compounds (for example, estradiol-17β [E2]) is protective. Further complexities are observed in humans ingesting anorexigens (female bias) and in rodent models, such as after hypoxia plus SU5416/Sugen (little sex bias) or involving serotonin transporter overexpression or dexfenfluramine administration (female bias). These complexities in sex bias in PH remain incompletely understood. We recently discovered that conditional deletion of signal transducer and activator of transcription 5a/b (STAT5a/b) in vascular smooth muscle cells abrogated the male bias in PH in hypoxic mice and that late-stage obliterative lesions in patients of both sexes with IPAH and HPAH showed reduced STAT5a/b, reduced Tyr-P-STAT5 and reduced B-cell lymphoma 6 protein (BCL6). In trying to understand the significance of these observations, we realized that there existed a wellcharacterized E2-sensitive central neuroendocrine mechanism of sex bias, studied over the last 40 years, that, at its peripheral end, culminated in species-specific male ("pulsatile") versus female ("more continuous") temporal patterns of circulating growth hormone (GH) levels leading to male versus female patterned activation of STAT5a/b in peripheral tissues and thus sex-biased expression of hundreds of genes. In this report, we consider the contribution of this neuroendocrine mechanism (hypothalamus-GH-STAT5) in the generation of sex bias in different PH situations.

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Understanding the control of ingestive behavior in primates

Cited by 10 publications

References 206 publications

Subjective social status is associated with compensation for large meals – A prospective pilot study

Subjective social status is associated with compensation for large meals – A prospective pilot study

Nutrient‐specific compensation for seasonal cold stress in a free‐ranging temperate colobine monkey

Hypothesis: Neuroendocrine Mechanisms (Hypothalamus-Growth Hormone-STAT5 Axis) Contribute to Sex Bias in Pulmonary Hypertension

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