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老年大鼠的口渴缺失可通过饮食补充 ω-3 脂肪酸得到逆转。

Thirst deficits in aged rats are reversed by dietary omega-3 fatty acid supplementation.

机构信息

School of Psychological Science, La Trobe University, Melbourne, Victoria, Australia.

出版信息

Neurobiol Aging. 2012 Oct;33(10):2422-30. doi: 10.1016/j.neurobiolaging.2011.12.001. Epub 2012 Jan 5.

Abstract

During heat waves many elderly individuals die as a consequence of dehydration. This is partially due to deficits in mechanisms controlling thirst. Reduced thirst following dipsogenic stimuli is well documented in aged humans and rodents. Low in vivo long-chain omega-3 fatty acid levels, as can occur in aging, have been shown to alter body fluid and sodium homeostasis. Therefore, the effect of dietary omega-3 fatty acid supplementation on drinking responses in aged rats was examined. Omega-3 fatty acids reversed thirst deficits in aged rats following dehydration and hypertonic stimuli; angiotensin (ANG) II induced drinking was unaffected in aged rats. Plasma atrial natriuretic peptide (ANP) and arginine vasopressin (AVP) were altered with age, but not affected by diet. Aged omega-3 fatty acid deficient animals displayed increased hypothalamic cytosolic phospholipase A(2) (cPLA(2)), cyclooxygenase (COX)-2, and prostaglandin E (PGE) synthase messenger (m)RNA expression, compared with animals that received omega-3 fatty acids. The aged low omega-3 fatty acid fed animals had significantly elevated hypothalamic PGE(2) compared with all other groups. Hypothalamic PGE(2) was negatively correlated with drinking induced by both dehydration and hypertonicity. The results indicate that PGE(2) may be the underlying mechanism of the reduced thirst observed in aging.

摘要

在热浪期间,许多老年人因脱水而死亡。这部分是由于控制口渴的机制缺陷所致。在老年人和啮齿动物中,已经充分证明了对饮水刺激的口渴反应减少。体内长链ω-3 脂肪酸水平降低(如衰老时发生的情况)会改变体液和钠稳态。因此,研究了饮食中ω-3 脂肪酸补充对老年大鼠饮水反应的影响。ω-3 脂肪酸可逆转脱水和高渗刺激后老年大鼠的口渴缺陷;血管紧张素(ANG)II 诱导的饮水在老年大鼠中不受影响。血浆心钠肽(ANP)和精氨酸加压素(AVP)随年龄而变化,但不受饮食影响。与接受ω-3 脂肪酸的动物相比,缺乏ω-3 脂肪酸的老年动物的下丘脑胞质型磷脂酶 A(2)(cPLA(2))、环加氧酶(COX)-2 和前列腺素 E(PGE)合酶信使(m)RNA 表达增加。与所有其他组相比,食用低ω-3 脂肪酸的老年动物的下丘脑 PGE(2)显着升高。下丘脑 PGE(2)与脱水和高渗性引起的饮水呈负相关。结果表明,PGE(2)可能是衰老时观察到的口渴减少的潜在机制。

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