Diurnal‐nocturnal changes in food intake, gut storage of ingesta, food transit time and metabolism in growing broiler chickens: A model for temporal control of energy balance

1993 ◽  
Vol 34 (4) ◽  
pp. 699-709 ◽  
Author(s):  
J. Buyse ◽  
D. S. Adelsohn ◽  
E. Decuypere ◽  
C. G. Scanes
Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 196-LB
Author(s):  
WENWEN C. CHENG ◽  
ERMELINDA NDOKA ◽  
BASMA MAERZ ◽  
KAREN J. ROELOFS ◽  
CHRISTOPHER J. RHODES ◽  
...  
Keyword(s):  

Appetite ◽  
1990 ◽  
Vol 14 (1) ◽  
pp. 67-69 ◽  
Author(s):  
Theresa A. Spiegel
Keyword(s):  

Endocrinology ◽  
2021 ◽  
Author(s):  
Katharina Schnabl ◽  
Yongguo Li ◽  
Mueez U-Din ◽  
Martin Klingenspor

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.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Irene Cimino ◽  
Debra Rimmington ◽  
Y. C. Loraine Tung ◽  
Katherine Lawler ◽  
Pierre Larraufie ◽  
...  

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.


2007 ◽  
Vol 99 (1) ◽  
pp. 212-213
Author(s):  
Andreas Zafeiridis ◽  
Vassilis Mougios

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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