In order to better understand the link between obesity and type 2 diabetes, lipolysis and its adrenergic regulation was investigated in various adipose depots of obese adult females SHR/N-cp rats. Serum insulin, glucose, free fatty acids (FFA), triglycerides (TG) and glycerol were measured. Adipocytes were isolated from subcutaneous (SC), parametrial (PM) and retroperitoneal (RP) fat pads. Total cell number and size, basal lipolysis or stimulated by norepinephrine (NE) and BRL 37344 were measured in each depot. Obese rats were hyperinsulinemic and hyperglycemic, suggesting high insulin resistance. They presented a marked dyslipidemia, attested by increased serum FFA and TG levels. High serum glycerol levels also suggest a strong lipolytic rate. Obese rats showed an excessive development of all fat pads although a more pronounced effect was observed in the SC one. The cellularity of this depot was increased 8 fold when compared to lean rats, but these fat cells were only 1.5 to 2-fold larger. SC adipocytes showed a marked increase in their basal lipolytic activity but a lack of change in responsiveness to NE or BRL 37344. The association between high basal lipolysis and increased cellularity yields to a marked adipose cell lipolytic rate, especially from the SC region. SHR/N-cp rats were characterized by a hyperplasic type of obesity with an excessive development of the SC depot. The dyslipidemia, attested by an altered serum lipid profile could be attributed to excessive lipolysis that contributes to increased FFA levels, and to early development of insulin resistance through a lipotoxicity effect.

中文翻译：

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自发性高血压/NIH 肥胖 (SHR/N-cp) 大鼠的高脂解活性和血脂异常：肥胖和 2 型糖尿病的遗传模型。

为了更好地了解肥胖与 2 型糖尿病之间的联系，在肥胖成年女性 SHR/N- cp 的各种脂肪库中研究了脂肪分解及其肾上腺素能调节老鼠。测量血清胰岛素、葡萄糖、游离脂肪酸 (FFA)、甘油三酯 (TG) 和甘油。从皮下 (SC)、宫旁 (PM) 和腹膜后 (RP) 脂肪垫中分离脂肪细胞。在每个仓库中测量总细胞数和大小、基础脂肪分解或由去甲肾上腺素 (NE) 和 BRL 37344 刺激。肥胖大鼠是高胰岛素血症和高血糖症，提示高胰岛素抵抗。他们表现出明显的血脂异常，通过增加的血清 FFA 和 TG 水平来证明。高血清甘油水平也表明脂肪分解率很高。肥胖大鼠显示所有脂肪垫过度发育，尽管在 SC 中观察到更明显的效果。与瘦大鼠相比，该仓库的细胞数量增加了 8 倍，但这些脂肪细胞仅大 1.5 到 2 倍。SC 脂肪细胞的基础脂肪分解活性显着增加，但对 NE 或 BRL 37344 的反应没有变化。高基础脂肪分解和细胞结构增加之间的关联导致显着的脂肪细胞脂肪分解率，尤其是来自 SC 区域。SHR/N-cp大鼠的特征是增生型肥胖，SC 库过度发育。由改变的血清脂质谱证明的血脂异常可归因于导致 FFA 水平增加的过度脂肪分解，以及通过脂毒性作用导致胰岛素抵抗的早期发展。