196-LB: Synergetic and Distinct Roles in the Control of Food Intake and Energy Balance for Subpopulations of NTS Neurons

Abstract The obesity pandemic requires effective preventative and therapeutic intervention strategies. Successful and sustained obesity treatment is currently limited to bariatric surgery. Modulating the release of gut hormones is considered promising to mimic bariatric surgery with its beneficial effects on food intake, body weight and blood glucose levels. The gut peptide secretin was the first molecule to be termed a hormone; nevertheless, it only recently has been established as a legitimate anorexigenic peptide. In contrast to gut hormones that crosstalk with the brain either directly or by afferent neuronal projections, secretin mediates meal-associated brown fat thermogenesis to induce meal termination, thereby qualifying this physiological mechanism as an attractive, peripheral target for the treatment of obesity. In this perspective, it is of pivotal interest to deepen our yet superficial knowledge on the physiological roles of secretin as well as meal-associated thermogenesis in energy balance and body weight regulation. Of note, the emerging differences between meal-associated thermogenesis and cold-induced thermogenesis must be taken into account. In fact, there is no correlation between these two entities. In addition, the investigation of potential effects of secretin in hedonic-driven food intake, bariatric surgery as well as chronic treatment using suitable application strategies to overcome pharmacokinetic limitations will provide further insight into its potential to influence energy balance. The aim of this article is to review the facts on secretin’s metabolic effects, address prevailing gaps in our knowledge, and provide an overview on the opportunities and challenges of the therapeutic potential of secretin in body weight control.

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Body energy balance and food intake: a neuroendocrine regulatory mechanism

Physiological Reviews ◽

10.1152/physrev.1983.63.1.314 ◽

1983 ◽

Vol 63 (1) ◽

pp. 314-386 ◽

Cited By ~ 146

Author(s):

J. Le Magnen

Keyword(s):

Energy Balance ◽

Food Intake ◽

Regulatory Mechanism ◽

Body Energy

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Development of Hypothalamic Circuits That Control Food Intake and Energy Balance

Appetite and Food Intake ◽

10.1201/9781315120171-7 ◽

2017 ◽

pp. 135-154 ◽

Cited By ~ 16

Author(s):

Sebastien G. Bouret

Keyword(s):

Energy Balance ◽

Food Intake ◽

Control Food ◽

Control Food Intake

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Murine neuronatin deficiency is associated with a hypervariable food intake and bimodal obesity

Scientific Reports ◽

10.1038/s41598-021-96278-8 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Irene Cimino ◽

Debra Rimmington ◽

Y. C. Loraine Tung ◽

Katherine Lawler ◽

Pierre Larraufie ◽

...

Keyword(s):

Body Weight ◽

Energy Balance ◽

Food Intake ◽

Energy Expenditure ◽

Positive Energy ◽

Chow Diet ◽

Chromatin Regulator ◽

Positive Energy Balance ◽

The Impact ◽

Deficient Mice

AbstractNeuronatin (Nnat) has previously been reported to be part of a network of imprinted genes downstream of the chromatin regulator Trim28. Disruption of Trim28 or of members of this network, including neuronatin, results in an unusual phenotype of a bimodal body weight. To better characterise this variability, we examined the key contributors to energy balance in Nnat+/−p mice that carry a paternal null allele and do not express Nnat. Consistent with our previous studies, Nnat deficient mice on chow diet displayed a bimodal body weight phenotype with more than 30% of Nnat+/−p mice developing obesity. In response to both a 45% high fat diet and exposure to thermoneutrality (30 °C) Nnat deficient mice maintained the hypervariable body weight phenotype. Within a calorimetry system, food intake in Nnat+/−p mice was hypervariable, with some mice consuming more than twice the intake seen in wild type littermates. A hyperphagic response was also seen in Nnat+/−p mice in a second, non-home cage environment. An expected correlation between body weight and energy expenditure was seen, but corrections for the effects of positive energy balance and body weight greatly diminished the effect of neuronatin deficiency on energy expenditure. Male and female Nnat+/−p mice displayed subtle distinctions in the degree of variance body weight phenotype and food intake and further sexual dimorphism was reflected in different patterns of hypothalamic gene expression in Nnat+/−p mice. Loss of the imprinted gene Nnat is associated with a highly variable food intake, with the impact of this phenotype varying between genetically identical individuals.

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Reply by Zafeiridis and Mougios

British Journal Of Nutrition ◽

10.1017/s0007114507761767 ◽

2007 ◽

Vol 99 (1) ◽

pp. 212-213

Author(s):

Andreas Zafeiridis ◽

Vassilis Mougios

Keyword(s):

Energy Balance ◽

Food Intake ◽

Resistance Exercise ◽

Tolerance Test ◽

Delayed Effect ◽

Exercise Protocol ◽

Postprandial Lipaemia ◽

Fat Tolerance Test

We thank Drs Burns and Stensel for their interest in our work. We agree that the published articles on the delayed effect of resistance exercise (RE) on postprandial lipaemia (PL) provide controversial results. Three studies1–3 employed comparable methodologies in terms of exercise protocol and feeding plan of the subjects, that is, two to four sets of eight to eleven exercises at relatively similar intensities (about 10–12 repetitions maximum (RM)) with 1·5–2·0 min of rest between sets and a standardised meal on the night prior to the fat tolerance test. These studies reported a decrease1,3 or no change2 in the postprandial lipaemic response. A fourth study4 employed a similar RE protocol but focused on maintaining the subjects in a state of energy balance by increasing food intake up to two-fold after RE v. control on the night prior to the fat tolerance test. This study found no significant effect of RE on PL.

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Glycomacropeptide, a low-phenylalanine protein isolated from cheese whey, supports growth and attenuates metabolic stress in the murine model of phenylketonuria

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00647.2011 ◽

2012 ◽

Vol 302 (7) ◽

pp. E885-E895 ◽

Cited By ~ 30

Author(s):

Patrick Solverson ◽

Sangita G. Murali ◽

Adam S. Brinkman ◽

David W. Nelson ◽

Murray K. Clayton ◽

...

Keyword(s):

Energy Balance ◽

Food Intake ◽

Energy Expenditure ◽

Lean Mass ◽

Metabolic Stress ◽

Casein Diet ◽

Wild Type ◽

Total Fat ◽

Spleen Mass ◽

Main Effects

Phenylketonuria (PKU) is caused by a mutation in the phenylalanine (phe) hydroxylase gene and requires a low-phe diet plus amino acid (AA) formula to prevent cognitive impairment. Glycomacropeptide (GMP) contains minimal phe and provides a palatable alternative to AA formula. Our objective was to compare growth, body composition, and energy balance in Pahenu2 (PKU) and wild-type mice fed low-phe GMP, low-phe AA, or high-phe casein diets from 3–23 wk of age. The 2 × 2 × 3 design included main effects of genotype, sex, and diet. Fat and lean mass were assessed by dual-energy X-ray absorptiometry, and acute energy balance was assessed by indirect calorimetry. PKU mice showed growth and lean mass similar to wild-type littermates fed the GMP or AA diets; however, they exhibited a 3–15% increase in energy expenditure, as reflected in oxygen consumption, and a 3–30% increase in food intake. The GMP diet significantly reduced energy expenditure, food intake, and plasma phe concentration in PKU mice compared with the casein diet. The high-phe casein diet or the low-phe AA diet induced metabolic stress in PKU mice, as reflected in increased energy expenditure and intake of food and water, increased renal and spleen mass, and elevated plasma cytokine concentrations consistent with systemic inflammation. The low-phe GMP diet significantly attenuated these adverse effects. Moreover, total fat mass, %body fat, and the respiratory exchange ratio (CO2 produced/O2 consumed) were significantly lower in PKU mice fed GMP compared with AA diets. In summary, GMP provides a physiological source of low-phe dietary protein that promotes growth and attenuates the metabolic stress induced by a high-phe casein or low-phe AA diet in PKU mice.

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Session 2: Calorie-Cutting Keys

Effective Weight Loss ◽

10.1093/med:psych/9780190232009.003.0002 ◽

2016 ◽

pp. 15-26

Author(s):

Evan M. Forman ◽

Meghan L. Butryn

Keyword(s):

Energy Balance ◽

Food Intake ◽

Eating Behavior ◽

Negative Energy ◽

Negative Energy Balance ◽

Calorie Intake ◽

Self Monitoring ◽

Serving Size ◽

High Calorie

This chapter (Session 2) discusses the importance of self-monitoring to gain awareness of calorie intake and to recognize patterns in eating behavior. Clients are provided with information on how to self-monitor food intake, including recording type of food, serving size, method of preparation, and time of eating. Strategies for beginning to reduce calories are discussed, such as limiting high-calorie foods in the environment, eating regular meals, and planning meals in advance. The idea of achieving a negative energy balance is introduced, meaning that in order to lose weight, clients must expend a greater amount of energy than they consume in the form of calories.

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