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首页> 外文期刊>Intensive Care Medicine Experimental >Proliferation and differentiation of adipose tissue in prolonged lean and obese critically ill patients
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Proliferation and differentiation of adipose tissue in prolonged lean and obese critically ill patients

机译：长期肥胖和肥胖重症患者的脂肪组织增殖和分化

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BackgroundIn prolonged non-obese critically ill patients, preservation of adipose tissue is prioritized over that of the skeletal muscle and coincides with increased adipogenesis. However, we recently demonstrated that in obese critically ill mice, this priority was switched. In the obese, the use of abundantly available adipose tissue-derived energy substrates was preferred and counteracted muscle wasting. These observations suggest that different processes are ongoing in adipose tissue of lean vs. overweight/obese critically ill patients. MethodsWe 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. 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. 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. ResultsThe 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. 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. 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. 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). ConclusionsContrary to what was hypothesized, adipogenesis increased independently of initial BMI in prolonged critically ill patients. Not the production of local eicosanoid PPARγ agonists but circulating adipogenic factors seem to be involved in critical illness-induced adipogenesis. 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.
机译：背景在长期的非肥胖重症患者中，脂肪组织的保存优先于骨骼肌的保存，并且与脂肪形成增加相吻合。但是，我们最近证明，在肥胖危重症小鼠中，该优先级已切换。在肥胖者中，首选使用大量可利用的脂肪组织来源的能量底物，以抵消肌肉的浪费。这些观察结果表明，瘦与超重/肥胖危重患者的脂肪组织中正在进行不同的过程。方法我们假设为了在危重疾病期间保持脂肪组织的质量，长期瘦身的危重病患者的脂肪形成会增加，而超重/肥胖的危重患者（脂肪过多的患者进入ICU）则不会增加脂肪形成。为了测试这一点，我们研究了在瘦弱者（n =？24）和超重/肥胖（n =？24）延长的重症患者皮下和内脏活检中脂肪形成的标志。其次，为了进一步揭示重大疾病引起的脂肪形成的潜在机制，研究了类花生酸PPARγ激动剂的局部产生，以及匹配的瘦肉（n = 20）和超重/肥胖（n = 20）血清的成脂潜力。 ）重病患者。结果瘦弱，超重/肥胖加重病患者的皮下和内脏脂肪组织活检中小脂肪细胞数量，PPARγ蛋白和CEBPB表达均上调（p≤？0.05）。与肥胖无关，与类花生酸生产有关的关键酶的基因表达降低（COX1，HPGDS，LPGDS，ALOX15，所有p≤0.05）或未改变（COX2，ALOX5）。在肥胖和超重/肥胖患者中，PLA2G2A和ALOX15B的基因表达上调（p≤？0.05），而在脂肪组织中其终产物PPARγ活化代谢产物15s-HETE和9-HODE却没有增加。在体外，瘦弱，超重/肥胖延长的重症患者血清平均刺激脂肪细胞增殖（p≤？0.05）和分化（脂质蓄积，DLK1和CEBPB表达，p≤？0.05）。结论与假设相反，在重症危重患者中，脂肪形成独立于最初的BMI增加。不是局部类花生酸PPARγ激动剂的产生，而是循环的成脂因子似乎与疾病诱发的严重成脂有关。重要的是，我们的发现表明，在严重疾病期间，来自脂肪组织的大量可用能量底物（而不是过多的脂肪细胞）可以发挥有益作用。

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