a Department of Biology , Adelphi University , Garden City, New York , New York , USA.
b Cross Island Lab , Mineola , New York , USA.
J Am Coll Nutr. 2018 May-Jun;37(4):328-335. doi: 10.1080/07315724.2017.1412276. Epub 2018 Mar 13.
To determine the hormonal changes that occur as a result of the long-term intake of a very-high-fat diet (VHFD) that leads to simultaneous changes in the islets of Langerhans and adipocyte cell size.
Male mice were fed with a normal chow diet (ND, n = 15) and a VHFD (n = 30) for 2, 12, and 24 weeks. Body weight, food intake, caloric intake (fat [saturated and unsaturated], protein, and carbohydrate), hormone levels (leptin and insulin), and islet of Langerhans/adipocyte size were quantitatively recorded.
In VHFD-fed animals, body weight showed a significant percent increase within the first 12 weeks and then plateaued with time. VHFD-fed animals consumed significantly less food than ND at all time periods, indicating that it was the quality of food and not the quantity that caused this increase in body weight. Male mice on VHFD showed a significant increase in leptin and insulin levels, along with accompanying growth in islet and adipocyte size within the first 12 weeks, which plateaued as the mice aged. The increases in the islet and adipocyte size in VHFD-fed animals were similar to the analogous increases in hormonal levels (2 vs. 12 vs. 24 weeks). These results, therefore, suggest that in diet-induced obesity changes, shifts in hormonal levels works hand-in-hand with metabolic adjustments at the cellular level to combat the effect of fat.
Thus, mechanisms like hormonal resistance, changes in adiposity, islet size, and caloric intake with prolonged exposure to high fat are probably defensive mechanisms employed to protect against diabetes. In order to understand these complicated and nuanced effects of high fat and to comprehend the underlying mechanism associated with it, it is important to focus on long-term studies that emphasize the synergy between cellular and hormonal changes, in addition to an analysis of individual components.
确定长期摄入极高脂肪饮食（VHFD）导致胰岛和脂肪细胞大小同时发生变化时所发生的激素变化。
雄性小鼠分别用正常饲料（ND，n=15）和 VHFD（n=30）喂养 2、12 和 24 周。定量记录体重、食物摄入量、热量摄入（脂肪[饱和和不饱和]、蛋白质和碳水化合物）、激素水平（瘦素和胰岛素）以及胰岛/脂肪细胞大小。
在 VHFD 喂养的动物中，体重在前 12 周内显著增加，然后随着时间的推移趋于稳定。VHFD 喂养的动物在所有时间段的食物摄入量均明显少于 ND，这表明导致体重增加的是食物的质量而不是数量。VHFD 喂养的雄性小鼠的瘦素和胰岛素水平显著升高，同时在最初的 12 周内胰岛和脂肪细胞大小也随之增长，随着小鼠年龄的增长而趋于稳定。VHFD 喂养动物的胰岛和脂肪细胞大小的增加与类似的激素水平增加（2 周、12 周、24 周）相似。因此，这些结果表明，在饮食诱导的肥胖变化中，激素水平的变化与细胞水平的代谢调整协同作用，以对抗脂肪的影响。
因此，长期暴露于高脂肪会导致激素抵抗、肥胖、胰岛大小和热量摄入的变化等机制，可能是为了防止糖尿病而采取的防御机制。为了理解高脂肪的这些复杂而微妙的影响，并理解与之相关的潜在机制，重要的是要关注强调细胞和激素变化协同作用的长期研究，以及对单个成分的分析。
