To determine whether it is possible to use diet to cause a loss of adipocytes, adipose tissue cellularity was examined in adult male rats subjected to unusually prolonged semistarvation. After 1 wk of total fast, rats were given a nutritionally inadequate glucose-electrolyte diet for up to 7 wk. This caused a 49% reduction of body weight, up to a 99% reduction in the weight of adipose tissue, and significant losses of total adipose tissue DNA content. Nevertheless, there was no evidence that fat cells had been lost. The number of fat cells in the right epididymal depots of the food-deprived rats equaled both the number seen in left depots after refeeding and the number seen in corresponding depots of nonfasted controls. Adipose tissue DNA synthesis, which declined 88% below control values during fasting, did increase as much as 2,000% above control values during refeeding. However, autoradiographs showed that the increase reflects only the replacement of lost endothelial and nonadipocyte mesenchymal cells; no labeled fat cell nuclei were found. Thus, severe, long-term food deprivation followed by refeeding causes loss and recovery of stromal-vascular cells in adipose tissue but no loss of fat cells.

To determine whether muscle disuse after a spinal cord injury (SCI) produces elevated markers of cellular senescence and induces markers of the senescence‐associated secretory phenotypes (SASPs) in paralyzed skeletal muscle. Four‐month‐old male Sprague‐Dawley rats received a moderate‐severe (250 kiloDyne) T‐9 contusion SCI or Sham surgery and were monitored over 2 weeks, and 1‐, 2‐, or 3 months. Animals were sacrificed via isoflurane overdose and terminal exsanguination and the soleus was carefully excised and snap frozen. Protein expression of senescence markers p53, p27, and p16 was determined from whole soleus lysates using Western immunoblotting and RT‐qPCR was used to determine the soleus gene expression of IL‐1α, IL‐1β, IL‐6, CXCL1, and TNFα. SCI soleus muscle displayed 2‐ to 3‐fold higher total p53 protein expression at 2 weeks, and at 1 and 2 months when compared with Sham. p27 expression was stable across all groups and timepoints. p16 protein expression was lower at 3 months in SCI versus Sham, but not earlier timepoints. Gene expression was relatively stable between groups at 2 weeks. There were Surgery x Time interaction effects for IL‐6 and TNFα mRNA expression but not for IL‐1α, IL‐1β, or CXCL1. There were no main effects for time or surgery for IL‐1α, IL‐1β, or CXCL1, but targeted t tests showed reductions in IL‐1α and CXCL1 in SCI animals compared to Sham at 3 months and IL‐1β was reduced in SCI animals compared to Sham animals at the 2‐month timepoint. The elevation in p53 does not appear consistent with the induction of SASP because mRNA expression of cytokines associated with senescence was not uniformly upregulated and, in some instances, was downregulated in the early chronic phase of SCI.