Mechanisms involved in cardiovascular and hydroelectrolytic changes in dehydrated high-fat-diet-fed rats.

IF 2.2 3区 医学 Q3 PHYSIOLOGY
Jéssica Matheus Sá, Marcos Vinícius Fernandes, Roberto Braz Pontes, Eduardo Colombari, José Vanderlei Menani, Débora Simões Almeida Colombari
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Abstract

Obesity is increasingly prevalent worldwide, and climate change is exacerbating water shortages, leading to dehydration. Both obesity and dehydration cause increased arterial pressure (AP), fluid electrolytic imbalance, and neuroinflammation. Thus, the present study aimed to verify the changes in the cardiovascular system, hydroelectrolytic balance, and microglia and neuronal activation in rats fed with a high-fat diet (HFD) in response to 24 h of water deprivation (WD) and the possible mechanisms involved. Male Holtzman rats (290-310 g) were fed with a standard diet (SD, 10% calories from fat) or HFD (46% calories from fat) for 6 wk before the WD experiments. Compared with WD SD rats, WD HFD rats presented a greater c-Fos immunolabeling in the subfornical organ (SFO) and supraoptic nucleus and greater microglial activation in SFO. WD-induced water intake was lower in HFD rats than in SD rats. WD HFD rats presented greater antidiuresis and lesser natriuresis than WD SD rats. Renal denervation did not change the antidiuresis or natriuresis observed in WD HFD- or SD-fed rats. The lower water intake in WD HFD rats might be due to neuroinflammation and/or decreased urinary output. The increase in AP after WD was similar between HFD and SD, but it is more dependent on angiotensin II type 1 (AT1) receptor activation in HFD rats. Overall, HFD rats seem less responsive to fluid and electrolyte balance responses to WD, highlighting the need for strategies to prevent dehydration in individuals with obesity, particularly during rising drought conditions worldwide.NEW & NOTEWORTHY Obesity and dehydration are common worldwide. Our study with an animal model found that changes in arterial pressure are linked to increased activation of the AT1 receptor in obese, dehydrated rats. The renal nerves appear unrelated to the significant decrease in urinary volume and sodium excretion in these animals. Neuroinflammation and reduced urine output may explain their lower water intake. These findings highlight the need for strategies to prevent dehydration in individuals with obesity.

肥胖症在全球日益普遍,气候变化加剧了水资源短缺,导致脱水。肥胖和脱水都会导致动脉压升高、水电解失衡和神经炎症。因此,本研究旨在验证以高脂肪饮食(HFD)喂养的大鼠在 24 小时缺水(WD)情况下心血管系统、水电解平衡以及小胶质细胞和神经元活化的变化及其可能的机制。雄性 Holtzman 大鼠(290-310 克)在缺水实验前用标准饮食(SD,10% 热量来自脂肪)或高脂饮食(46% 热量来自脂肪)喂养 6 周。与 WD SD 大鼠相比,WD HFD 大鼠的角膜下器官(SFO)和视上核中出现了更多的 c-Fos 免疫标记,SFO 中的小胶质细胞活化程度更高。WD诱导的水摄入量在HFD大鼠中低于SD大鼠。与 WD SD 大鼠相比,WD HFD 大鼠表现出更强的抗利尿能力和更弱的利钠能力。肾脏去神经化并没有改变在 WD HFD 或 SD 喂养大鼠身上观察到的抗利尿或纳尿性。WD HFD 大鼠较低的水摄入量可能是由于神经炎症和/或排尿量减少所致。WD 后 AP 的增加在 HFD 和 SD 大鼠中相似,但在 HFD 大鼠中更依赖于 AT1 受体的激活。总之,高脂血症大鼠对WD的液体和电解质平衡反应似乎不太敏感,这突出表明需要制定策略来防止肥胖者脱水,尤其是在全球干旱加剧的情况下。
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来源期刊
CiteScore
5.30
自引率
3.60%
发文量
145
审稿时长
2 months
期刊介绍: The American Journal of Physiology-Regulatory, Integrative and Comparative Physiology publishes original investigations that illuminate normal or abnormal regulation and integration of physiological mechanisms at all levels of biological organization, ranging from molecules to humans, including clinical investigations. Major areas of emphasis include regulation in genetically modified animals; model organisms; development and tissue plasticity; neurohumoral control of circulation and hypertension; local control of circulation; cardiac and renal integration; thirst and volume, electrolyte homeostasis; glucose homeostasis and energy balance; appetite and obesity; inflammation and cytokines; integrative physiology of pregnancy-parturition-lactation; and thermoregulation and adaptations to exercise and environmental stress.
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