Fish Physiology and Biochemistry Division, ICAR-Central Institute of Fisheries Education, Off-Yari Road, Versova, Andheri (W), Mumbai, 400061, India.
Department of Aquaculture, Kerala University of Fisheries and Ocean Studies, Kochi, 682 506, India.
Fish Physiol Biochem. 2020 Feb;46(1):199-212. doi: 10.1007/s10695-019-00708-4. Epub 2019 Oct 21.
The Indian major carp, mrigal (Cirrhinus mrigala), is a bottom-dwelling fish that can survive hypoxic episodes in its natural environment. We hypothesise that it can better survive hypoxic conditions by altering metabolic responses through GABA (Gamma-aminobutyric acid) supplementation. In the first experiment, the hypoxia tolerance time of the fishes was evaluated under extreme anoxic conditions after feeding with GABA, which showed that GABA had improved survival time under hypoxia. To study the response of dietary GABA in hypoxia-exposed fish, the branchial HIF-1α expression levels, serum thyroid hormone levels and hepatic metabolic responses were assessed in the subsequent experiment. The treatment groups were fed for 60 days with experimental diets containing 4 levels of GABA (0.00% G, 0.50% G, 0.75% G and 1.0%G) and were subjected to 72-h hypoxia exposure (0.5 ± 0.02 mg L dissolved oxygen (DO)) whereas a control group was maintained under normoxic conditions (6.0 ± 0.21 mg L DO). The five treatment groups with three replicates were C0 (0% G + normoxia), H0 (0% G + hypoxia), H0.5 (0.50% G + hypoxia), H0.75 (0.75% G + hypoxia) and H1.0 (1.00% G + hypoxia). The results indicated that GABA supplementation triggered downregulation of HIF 1 alpha expression. When compared with the control group, decreased thyroxine (T4) and triiodothyronine (T3) levels were observed in the GABA-fed hypoxic groups. However, TSH (thyroid stimulating hormone) level remained unchanged in all the treatments. The LDH (lactate dehydrogenase) level in hypoxia-exposed groups was decreased by GABA supplementation. Our study demonstrated that GABA supplementation restores acute hypoxia-induced HIF-1α expression, thyroid hormone levels and LDH activities. On the other hand, it enhanced the citrate synthase (CS) activities at 0.5-1.00%, which showed a sharp decline in hypoxia. Hypoxia caused increase in the serum metabolites such as glucose, lactate, cholesterol and triglycerides. However, GABA supplementation was partially effective in reducing glucose and lactate level while triglycerides and cholesterol values remained unchanged. Overall, our results suggested a potential role of GABA in suppressing metabolism during hypoxia exposure, which can increase the chances of survival of the species Cirrhinus mrigala during hypoxia.
印度鲤鱼，鲤鱼（Cirrhinus mrigala），是一种底栖鱼类，可以在其自然环境中耐受缺氧期。我们假设，通过补充 GABA 改变代谢反应，它可以更好地在缺氧条件下生存。在第一个实验中，在喂食 GABA 后，在极端缺氧条件下评估鱼类的耐缺氧时间，结果表明 GABA 提高了缺氧条件下的生存时间。为了研究膳食 GABA 在缺氧暴露鱼类中的反应，在随后的实验中评估了鳃 HIF-1α表达水平、血清甲状腺激素水平和肝代谢反应。实验组用含有 4 种 GABA 水平（0.00%G、0.50%G、0.75%G 和 1.0%G）的实验饲料喂养 60 天，并进行 72 小时的缺氧暴露（0.5±0.02mg L 溶解氧（DO）），而对照组则维持在正常氧条件下（6.0±0.21mg L DO）。有三个重复的五个处理组为 C0（0%G+正常氧）、H0（0%G+缺氧）、H0.5（0.50%G+缺氧）、H0.75（0.75%G+缺氧）和 H1.0（1.00%G+缺氧）。结果表明，GABA 补充剂触发了 HIF 1α表达的下调。与对照组相比，在 GABA 喂养的缺氧组中观察到甲状腺素（T4）和三碘甲状腺原氨酸（T3）水平降低。然而，所有处理中 TSH（甲状腺刺激激素）水平保持不变。缺氧暴露组的 LDH（乳酸脱氢酶）水平因 GABA 补充而降低。我们的研究表明，GABA 补充剂恢复了急性缺氧诱导的 HIF-1α表达、甲状腺激素水平和 LDH 活性。另一方面，它在 0.5-1.00%时增强了柠檬酸合酶（CS）的活性，在缺氧时急剧下降。缺氧引起血清代谢物如葡萄糖、乳酸、胆固醇和甘油三酯的增加。然而，GABA 补充剂在降低葡萄糖和乳酸水平方面部分有效，而甘油三酯和胆固醇值保持不变。总的来说，我们的结果表明 GABA 在抑制缺氧暴露期间的代谢方面可能发挥作用，这可以增加鲤鱼在缺氧期间的生存机会。
