An analysis of the aberdeen center for energy regulation and obesity

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An analysis of the aberdeen center for energy regulation and obesity

Dr Nimesh Mody | Staff Profile | The Institute of Medical Sciences | The University of Aberdeen

Food deprivation 48 h reduced SOCS3 gene expression in hamsters acclimated to either long LD or short SD photoperiods, suggesting that leptin signals acute starvation regardless of photoperiod. Our results suggest that the development of leptin resistance in LD-acclimated hamsters involves SOCS3-mediated suppression of leptin signaling in the arcuate nucleus.

Increased SOCS3 expression in LD hamsters is independent of body fat and serum leptin levels, suggesting that the photoperiod is able to trigger the biannual reversible switch in leptin sensitivity. MUCH OF OUR knowledge about the roles of leptin and other peripheral and central signals involved in the regulation of body weight has come from studies of genetically obese mice and rats or from models of imposed negative energy balance.

However, our knowledge of the dynamic long-term regulation of body weight remains limited. A fascinating model for studies in this field is presented by the seasonal mammal, Phodopus sungorus, which shows a remarkable natural body weight cycle determined by the prevailing photoperiod.

Short day exposure SDeither as a gradual change natural conditions or as an abrupt change laboratory conditionsleads to a progressive reduction in body weight.

Associated with the loss in body fat is a decreased level of leptin gene expression in fat 23 and lowered serum leptin concentration 1.

Associated Data

A paradoxical situation is thus evident, where long day LD -acclimated hamsters with comparatively high endogenous leptin levels show a higher level of food intake 1 despite the purported anorexigenic leptin signal. This implies some resistance to the biological effects of this hormone in a LD summer photoperiod.

Furthermore, Klingenspor et al. However, the neuroendocrine basis of photoperiod-induced changes in leptin sensitivity is not known. The arcuate nucleus of the hypothalamus ARC is probably the most important integrative center for mediation of the leptin signal 4.

Central transduction of the leptin signal is mediated by the long form of the leptin receptor LRb 5activation of which results in autophosphorylation of the associated Janus kinase type 2 tyrosine kinase and the transmission of downstream phosphotyrosine-dependent signals.

The transcription factor, signal transducer and activator of transcription-3 STAT3is the most potent intracellular mediator of the leptin signal. Once activated, STAT3 regulates the transcription of leptin-responsive target genes.

One particular target gene is SOCS3 suppressor of cytokine signalinga broadly acting suppressor of cytokine signaling 6 that suppresses signaling downstream of the receptor by inhibition of STAT3 phosphorylation.

SOCS3 has been identified as a potential mediator of central leptin resistance 78. The hypothesis underlying the present study is that changes in leptin signaling pathways mediated by the inhibitory peptide SOCS3 may be critical to the physiological changes in body weight in the Siberian hamster.

We hypothesize that photoperiod has a direct effect on the leptin signaling system at the level of signal transduction, whereby reduced arcuate nucleus SOCS3 expression in SD hamsters activates leptin signaling.

Lower SOCS3 expression as an early response to SD could lead to an increased anorexigenic action of leptin levels and trigger the weight loss or growth restriction induced by SD.

Here, we address this hypothesis in a series of experiments with hamsters subjected to energetic and hormonal challenges to characterize the impact of energy balance, photoperiod, and leptin on SOCS3 mRNA.

Materials and Methods Animals All procedures involving animals were licensed under the Animals Scientific Procedures Act of and received approval from the ethical review committee at the Rowett Research Institute.

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All experimental animals were drawn from the Rowett breeding colony of Siberian hamsters 9 — 11 and were gestated and suckled in an LD photoperiod h light, 8-h dark cycle. All hamsters were weaned at 3 wk of age and were individually housed either at weaning or, in the case of adult animals, at least 2 wk before photoperiod manipulation.

Where specified, hamsters were maintained in a SD photoperiod 8-h light, h dark cyclebut with all other environmental conditions unaltered. Food Labsure pelleted diet, Special Diet Services, Witham, UK and water were available ad libitum unless specified otherwise, and rooms were maintained at 22 C.

All animals were killed by cervical dislocation in the middle of the light phase, and brains were rapidly removed and frozen on dry ice. Experimental protocols Experiment 1: Twenty-four female hamsters were divided into two groups of 12 at weaning, one of which was transferred to SD.

Archived brain sections were used from juvenile female hamsters killed at weaning or 4, 7, 14, or 21 d postweaning in either photoperiod As before, all animals were gestated and weaned in LD, with transfer to SD at weaning, as appropriate.

The protocol employed was similar to that previously described for adult males 10except that the restriction periods were of either 6-wk experiment 3a or wk experiment 3b duration.

An analysis of the aberdeen center for energy regulation and obesity

For each study duration, hamsters were allocated to one of three groups. Body weight and food intake were measured daily for all animals during the restriction period.

After 6 wk experiment 3a or 12 wk experiment 3bhamsters were killed, trunk blood was collected in lithium-heparin tubes, and brains were removed and frozen on dry ice.

The total mass of the dissected white adipose tissue depots was taken as a measure of body adiposity. Forty-eight juvenile female hamsters were allocated to two weight-matched groups of 24 animals, one of which was transferred to SD for 8 wk.

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Twenty-four adult male hamsters, 4—6 months of age, were allocated to two weight-matched groups of 12 animals, one of which was transferred into SD for 12 wk.

A riboprobe complementary to the suppressor of cytokine signaling-3 SOCS3 was generated from cloned cDNA from the hypothalamus of the Siberian hamster.

The amplification was performed using the following primers: One slide from each animal was hybridized. Slides were treated with ribonuclease A, desalted, with a final high stringency wash 30 min in 0. Autoradiographic images were quantified using the Image-Pro Plus system version 4.

Equivalent sections of individual animals were matched according to the atlas of the mouse brain.An analysis of the aberdeen center for energy regulation and obesity newspapers.

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The Aberdeen Centre for Energy Regulation and Obesity (ACERO) brings together experts from the Rowett Research Institute, the University of Aberdeen, and the Grampian University Hospitals NHS Trust to share their knowledge, and vision for the future. Trends of body weight, energy intake, energy expenditure, absolute protein intake, and the activity of aminopeptidase in the perfect protein leverage model (A), the perfect energy regulation model (B), a mixed model of protein leverage and energy regulation (C), and the hedonic overdrive model (D).

Obesity and Metabolic Health Division, Aberdeen Centre for Energy Balance and Obesity, Rowett Research Institute, Bucksburn, Aberdeen, United Kingdom Submitted 21 March ; accepted in final form 13 April Understanding and addressing the epidemic of obesity: An energy balance perspective.

Hill, JO. Hill, JO. Center for Human Nutrition, University of Colorado School of Medicine, Denver, Colorado. Effects of Body Mass and Reproduction on the Basal Metabolic Rate of Brown Long‐Eared Bats (Plecotus auritus) Scotland; 2 Aberdeen Centre for Energy Regulation and Obesity, Department of Zoology, University of Aberdeen, Aberdeen AB24 2TZ, Scotland.

An analysis of the aberdeen center for energy regulation and obesity
PIXImus DXA with different software needs individual calibration to accurately predict fat mass.