Adipocyte development and insulin resistance

脂肪垫在能量过剩和不足时动态调节能量储存能力。这种重塑过程尚未完全理解，关于脂肪库和脂肪细胞数量可塑性之间的差异存在争议。 我们先前研究了小鼠脂肪细胞大小分布的变化，在附睾，腹股沟，腹膜后，和肠系膜脂肪下的体重增加和损失。通过数学建模，我们具体分析了脂肪细胞的招募，生长/收缩和损失，包括这些过程的大小依赖性。我们在所有四个脂肪库中发现了一个定性的普遍脂肪组织重塑过程：（1）体重增加时不断招募新细胞;（2）较大细胞（直径> 50微米）的生长和收缩与细胞表面积成比例;（3）在长期体重增加时发生细胞损失，较大细胞更容易受到影响。该数学模型给出了脂肪组织重塑的预测性综合图，并可用于检查这些特定细胞过程在肥胖和糖尿病中的相对重要性的变化。 在体重增加的情况下，脂肪垫不断招募新的脂肪细胞。 大脂肪细胞的生长/收缩与其表面积成正比。 较大的脂肪细胞在长时间的体重增加下更容易受到细胞损失。 在以前的出版物中，我们表明，似乎有一个周期性的细胞大小的概率分布的变化，通过分析纵向数据从两个Zucker脂肪大鼠。在这项工作中，我们提出了一个数学模型，可以产生这样的周期性，该模型的预测是，高脂肪饮食可能会导致相对于食物的周期缩短。我们的合作者（Cushman博士实验室的Mathilde Arroyo）在Zucker脂肪大鼠中进行了实验，我们一直在分析所得数据以验证我们的预测。看起来，这个新数据集的可变性可能掩盖了预测所建议的形式的任何规律性。这项工作正在进行中。

Fat pads dynamically regulate energy storage capacity under energy excess and deficit. This remodeling process is not completely understood, with controversies regarding differences between fat depots and plasticity of adipose cell number. We previously examined changes of mouse adipose cell-size distributions in epididymal, inguinal, retroperitoneal, and mesenteric fat under both weight gain and loss. With mathematical modeling, we specifically analyzed the recruitment, growth/shrinkage, and loss of adipose cells, including the size dependence of these processes. We found a qualitatively universal adipose tissue remodeling process in all four fat depots: (1) There is continuous recruitment of new cells under weight gain; (2) The growth and shrinkage of larger cells (diameter > 50 microns) is proportional to cell surface area; and (3) Cell loss occurs under prolonged weight gain, with larger cells more susceptible. The mathematical model gives a predictive integrative picture of adipose tissue remodeling, and can be used to examine changes in the relative importance of these specific cellular processes in obesity and diabetes. Fat pads continuously recruited new adipose cells under weight gain. Growth/shrinkage of large adipose cells is proportional to their surface area. Larger adipose cells are more susceptible to cell loss under prolonged weight gain. In previous publications, we demonstrated that there appeared to be a periodicity in changes in the cell-size probability distributions by analyzing longitudinal data from two Zucker fatty rats. In that work, we proposed a mathematical model that could give rise to such periodicity, and a prediction of that model was that a high-fat diet may lead to a decrease in the period, relative to chow. Our collaborator (Mathilde Arroyo in Dr. Cushman's laboratory) carried out experiments in Zucker fatty rat, and we have been analyzing the resulting data to test our prediction. It appears that the variability in this new dataset may mask the appearance of any regularity of the form suggested by the prediction. This work is ongoing.