Abstract
In maturing rats, the growth of abdominal fat is attenuated by voluntary wheel running. After the cessation of running by wheel locking, a rapid increase in adipose tissue growth to a size that is similar to rats that have never run (i.e. catch-up growth) has been previously reported by our lab. In contrast, diet-induced increases in adiposity have a slower onset with relatively delayed transcriptomic responses. The purpose of the present study was to identify molecular pathways associated with the rapid increase in adipose tissue after ending 6 wks of voluntary running at the time of puberty. Age-matched, male Wistar rats were given access to running wheels from 4 to 10 weeks of age. From the 10th to 11th week of age, one group of rats had continued wheel access, while the other group had one week of wheel locking. Perirenal adipose tissue was extracted, RNA sequencing was performed, and bioinformatics analyses were executed using Ingenuity Pathway Analysis (IPA). IPA was chosen to assist in the understanding of complex ‘omics data by integrating data into networks and pathways. Wheel locked rats gained significantly more fat mass and significantly increased body fat percentage between weeks 10–11 despite having decreased food intake, as compared to rats with continued wheel access. IPA identified 646 known transcripts differentially expressed (p < 0.05) between continued wheel access and wheel locking. In wheel locked rats, IPA revealed enrichment of transcripts for the following functions: extracellular matrix, macrophage infiltration, immunity, and pro-inflammatory. These findings suggest that increases in visceral adipose tissue that accompanies the cessation of pubertal physical activity are associated with the alteration of multiple pathways, some of which may potentiate the development of pubertal obesity and obesity-associated systemic low-grade inflammation that occurs later in life.
Highlights
The U.S Centers for Disease Control and Prevention has reported that the overall prevalence of obesity among U.S youth remains high (16.9%)
The purpose of the current study was to employ unbiased transcriptomics to determine which cellular and metabolic pathways might be altered during LOCK, and may provide insight into the initial mechanisms by which obesity is facilitated, when food intake is paradoxically falling to help in explaining the rapid increase in perirenal adipose tissue (PRAT)
PRAT adipocyte diameters were significantly greater in LOCK (67.1 ± 1.4) compared to RUN (62.2 ± 3.9) (p < 0.05); adipocyte cell number was estimated to be significantly increased in PRAT in LOCK compared to RUN (24.2 x 106 vs 14.9 x 106, p < 0.05)
Summary
The U.S Centers for Disease Control and Prevention has reported that the overall prevalence of obesity among U.S youth remains high (16.9%). To address questions surrounding the influence of decreased energy expenditure on early obesity development in physically-active animals, our laboratory developed a unique polygenic model by which rats are provided voluntary physical activity (access to wheel running) for a given period of time, which is immediately followed by days of no physical activity by locking running wheels [wheel lock (LOCK)] [1,2,3,4]. In this model, young rats with continuous access to a voluntary running wheel exhibit lower intra-abdominal adipose tissue levels than rats without wheels. Upon cessation of voluntary running by LOCK, three sequential caloric events occur [1, 2]: 1) an inferred, decreased energy expenditure from cessation of voluntary running; 2) a rapid 2–3 day decrease in ad libitum caloric intake from rats with continued free wheel access (RUN); and 3) a rapid increase in intra-abdominal adipose tissue mass to levels of age-matched sedentary rats
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