However, as the muscle-sparing effect coincided with a decrease in adipose tissue mass, one could also interpret an increase in adipogenesis as an undesirable preservation of adipose tissue over the skeletal muscle. As it appears that having abundantly available adipose tissue is beneficial during critical illness, an increase in adipogenesis could be interpreted as an attempt to ensure sufficient adipose tissue during critical illness. overweight/obese critically ill patients. Overall, these findings indicate an essential role for the adipose tissue during critical illness but also suggest that different processes are ongoing in lean vs. These observations suggest that in overweight/obese critically ill patients, preservation of the adipose tissue is not prioritized but that the stored lipids in the adipose tissue are being used, which provokes a muscle-sparing effect. Obese critically ill mice lost relatively more adipose tissue mass than lean mice but ultimately retained more adipose tissue. Recently, we have shown in an animal and patient study that premorbid obesity protected against muscle wasting and weakness. Such preservation of adipose tissue mass during prolonged critical illness coincided with increased adipogenesis, as has been observed in subcutaneous and visceral adipose tissue biopsies of prolonged critically ill patients. Remarkably, in non-obese patients, critical illness prioritizes the maintenance of adipose tissue over skeletal muscle tissue. Importantly, our findings suggest that abundantly available energy substrates from the adipose tissue, rather than excess adipocytes, can play a beneficial role during critical illness.Ĭritical illness induces a hypercatabolic response with severe wasting of lean tissue. Not the production of local eicosanoid PPARγ agonists but circulating adipogenic factors seem to be involved in critical illness-induced adipogenesis. ConclusionsĬontrary to what was hypothesized, adipogenesis increased independently of initial BMI in prolonged critically ill patients. In vitro, serum of lean and overweight/obese prolonged critically ill patients equally stimulated adipocyte proliferation ( p ≤ 0.05) and differentiation (lipid accumulation, DLK1, and CEBPB expression, p ≤ 0.05). Gene expression of PLA2G2A and ALOX15B was upregulated in lean and overweight/obese patients ( p ≤ 0.05), whereas their end products, the PPARγ-activating metabolites 15s-HETE and 9-HODE, were not increased in the adipose tissue. Gene expression of key enzymes involved in eicosanoid production was reduced ( COX1, HPGDS, LPGDS, ALOX15, all p ≤ 0.05) or unaltered ( COX2, ALOX5) during critical illness, irrespective of obesity. The number of small adipocytes, PPARγ protein, and CEBPB expression were equally upregulated ( p ≤ 0.05) in subcutaneous and visceral adipose tissue biopsies of lean and overweight/obese prolonged critically ill patients. Secondly, to further unravel the underlying mechanism of critical illness-induced adipogenesis, local production of eicosanoid PPARγ agonists was explored, as well as the adipogenic potential of serum from matched lean ( n = 20) and overweight/obese ( n = 20) critically ill patients. To test this, we studied markers of adipogenesis in subcutaneous and visceral biopsies of matched lean ( n = 24) and overweight/obese ( n = 24) prolonged critically ill patients. We hypothesize that to preserve adipose tissue mass during critical illness, adipogenesis is increased in prolonged lean critically ill patients, but not in overweight/obese critically ill patients, who enter the ICU with excess adipose tissue. ![]() These observations suggest that different processes are ongoing in adipose tissue of lean vs. In the obese, the use of abundantly available adipose tissue-derived energy substrates was preferred and counteracted muscle wasting. However, we recently demonstrated that in obese critically ill mice, this priority was switched. In prolonged non-obese critically ill patients, preservation of adipose tissue is prioritized over that of the skeletal muscle and coincides with increased adipogenesis.
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