HOPE Cardiometabolic Research Team & Department of Physiology, College of Health Sciences, University of Ilorin, Ilorin, Nigeria; Department of Physiology, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria.
HOPE Cardiometabolic Research Team & Department of Physiology, College of Health Sciences, University of Ilorin, Ilorin, Nigeria.
Nutrition. 2020 Sep;77:110789. doi: 10.1016/j.nut.2020.110789. Epub 2020 Mar 6.
Mishandling of lipid and glycogen has been documented as a feature of metabolic tissues in insulin resistance-related disorders. However, reports exist detailing that L-glutamine (GLN) protects non-adipose tissue against the deleterious effects of metabolic disorders. Therefore, we hypothesized that GLN would protect skeletal muscle and adipose tissue against the deleterious effects of lipid and glycogen mishandlings by increasing adenosine and glutathione levels in pregnant rats exposed to fructose (FRU)-enriched drinks.
Pregnant Wistar rats weighing 150 to 180 g were randomly assigned to control, GLN, FRU, and FRU + GLN groups (six rats/group). The groups received vehicle (P.o.), glutamine (1 g/kg), FRU (10%; w/v), and FRU + GLN, respectively, for 19 d.
Data show that FRU caused insulin resistance with corresponding increased blood glucose, circulating and pancreatic insulin levels, and lipid accumulation and glycogen depletion in skeletal muscle, but glycogen accumulation and a decreased lipid profile in adipose tissue. Adenosine and glutathione content decreased, whereas adenosine deaminase, xanthine oxidase, uric acid, and malondialdehyde concentrations increased in both tissues. In addition, glucose-6-phosphate dehydrogenase activity decreased in skeletal muscle but remained unaltered in adipose tissue. However, supplementation with GLN improved perturbed lipid and glycogen with a corresponding increase in adenosine and glutathione.
The present results collectively indicate that lipid and glycogen mishandlings caused by high gestational FRU intake result in the depletion of adenosine and glutathione in skeletal muscle and adipose tissue. These findings also suggest that L-glutamine protects against skeletal muscle and adipose tissue dysmetabolism by enhancing adenosine and glutathione.
代谢组织中脂类和糖原处理不当已被证明是与胰岛素抵抗相关疾病的特征。然而，有报道详细描述了 L-谷氨酰胺（GLN）可保护非脂肪组织免受代谢紊乱的有害影响。因此，我们假设 GLN 通过增加腺苷和谷胱甘肽水平，可保护骨骼肌和脂肪组织免受脂质和糖原处理不当对怀孕大鼠的有害影响，这些大鼠暴露于富含果糖（FRU）的饮料中。
体重为 150 至 180 g 的 Wistar 孕鼠被随机分为对照组、GLN 组、FRU 组和 FRU + GLN 组（每组 6 只）。这些组分别接受载体（p.o.）、谷氨酰胺（1 g/kg）、FRU（10%（w/v））和 FRU + GLN，共 19 天。
数据显示，FRU 导致胰岛素抵抗，伴有相应的血糖、循环和胰腺胰岛素水平升高，以及骨骼肌中脂质积累和糖原耗竭，但脂肪组织中糖原积累和脂质谱降低。两种组织中的腺苷和谷胱甘肽含量降低，而腺苷脱氨酶、黄嘌呤氧化酶、尿酸和丙二醛浓度增加。此外，葡萄糖-6-磷酸脱氢酶活性在骨骼肌中降低，但在脂肪组织中保持不变。然而，GLN 补充可改善紊乱的脂质和糖原，相应地增加腺苷和谷胱甘肽。
本研究结果表明，高妊娠 FRU 摄入导致骨骼肌和脂肪组织中腺苷和谷胱甘肽耗竭，从而导致脂质和糖原处理不当。这些发现还表明，L-谷氨酰胺通过增强腺苷和谷胱甘肽来保护骨骼肌和脂肪组织的代谢紊乱。
