L-tryptophan effectively prevents fatty degeneration of rat pancreas

R. Yanko, O. G. Chaka, M. Levashov
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Abstract

Alimentary obesity is a risk factor for the development of many pathophysiological conditions in various organs, including the pancreas. Thus, the study of mechanisms, clinical symptoms and ways to prevent the development of fatty degeneration of pancreas at obesity is a current direction of research. The aim of our work was to study the influence of L-tryptophan on the morphofunctional changes of the pancreas of rats with diet-induced obesity and to evaluate the possibility of its use for the prevention of the development of the gland fatty degeneration. The study was conducted in male Wistar rats, which were 3 months old at the experiment beginning. Histologic preparations were made from pancreas tissue samples using a standard method. Morphometric measurements were performed on digital images using “Image J” software. In biochemical studies, we determined concentration of glucose in blood serum and of triglycerides, lipids and cholesterol in pancreas tissue samples. It was found that rats fed a high-fat, high-carbohydrate diet showed marked sings of developing alimentary obesity. This was evidenced by a significant increase in the weight of visceral fat (by 147%) and obesity index (by 129%). The exposure of rats to a high-calorie diet resulted in the emergence of distinct signs indicating hypofunction in both the exocrine and, to a greater extent, endocrine sections of the pancreas. The administration of L-tryptophan reduced the intensity of accumulation of visceral fat and fat in the gland itself. This was evidenced by lower concentrations of lipids (by 53%) and triglycerides (by 32%) in the pancreatic tissue compared to high-calorie diet rats. In addition, L-tryptophan prevented an excessive decrease in the function of both the exocrine and endocrine parts of the gland from the harmful effects of dietary obesity. This may be of practical interest when using tryptophan and its derivatives in the clinic to prevent a decrease in gland activity in this pathology.
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左旋色氨酸可有效防止大鼠胰腺脂肪变性
膳食肥胖是包括胰腺在内的各种器官发生多种病理生理状况的危险因素。因此,研究肥胖导致胰腺脂肪变性的机制、临床症状和预防方法是当前的研究方向。我们的工作旨在研究 L-色氨酸对饮食诱导肥胖大鼠胰腺形态功能变化的影响,并评估其用于预防腺体脂肪变性发展的可能性。研究对象是实验开始时 3 个月大的雄性 Wistar 大鼠。采用标准方法对胰腺组织样本进行组织学制备。使用 "Image J "软件对数字图像进行形态测量。在生化研究中,我们测定了血清中葡萄糖的浓度以及胰腺组织样本中甘油三酯、脂类和胆固醇的浓度。研究发现,以高脂肪、高碳水化合物饮食喂养的大鼠表现出明显的消化道肥胖症。这表现在内脏脂肪重量(增加 147%)和肥胖指数(增加 129%)显著增加。大鼠摄入高热量饮食后,会出现明显的迹象,表明胰腺外分泌功能减退,在更大程度上也表明胰腺内分泌功能减退。服用 L-色氨酸可减少内脏脂肪和胰腺本身脂肪的堆积。与高热量饮食大鼠相比,胰腺组织中的脂质浓度(降低 53%)和甘油三酯浓度(降低 32%)均有所降低。此外,L-色氨酸还能防止胰腺的外分泌和内分泌功能因饮食肥胖的有害影响而过度下降。在临床上使用色氨酸及其衍生物来防止这种病症导致的腺体活动下降时,这可能具有实际意义。
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