Chronic whole-body heat treatment in obese insulin-resistant C57BL/6J mice.

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM Archives of Physiology and Biochemistry Pub Date : 2024-09-26 DOI:10.1080/13813455.2024.2406904

Helena Trevisan Schroeder, Carlos Henrique de Lemos Muller, Maria Inês Lavina Rodrigues, Marcela Alves de Azevedo, Victor de Souza Borges, Cristiana Maria Sponchiado, Paulo Ivo Homem de Bittencourt

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Abstract

Aim: This study examined the effects of hyperthermic therapy (HT) on mice fed normal chow or a high-fat diet (HFD) for 18 or 22 weeks, undergoing four or eight weekly HT sessions.

Methods: Mice were housed within their thermoneutral zone (TNZ) to simulate a physiological response. HFD-induced obesity-related changes, including weight gain, visceral fat accumulation, muscle loss (indicative of obesity sarcopenia), glucose intolerance, and hepatic triglyceride buildup.

Main results: HT upregulated HSP70 expression in muscles, mitigated weight gain, normalised QUICK index, and reduced plasma HSP70 concentrations. It also lowered the H-index of HSP70 balance, indicating improved immunoinflammatory status, and decreased activated caspase-1 and proliferative senescence in adipose tissue, both linked to insulin resistance.

Conclusion: The findings suggest that even animals on a "control" diet but with insufficient physical activity and within their TNZ may experience impaired glycaemic homeostasis.

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对肥胖的胰岛素抵抗型 C57BL/6J 小鼠进行慢性全身热处理。

目的：本研究考察了热疗（HT）对喂食正常饲料或高脂饮食（HFD）18周或22周的小鼠的影响，每周进行四次或八次热疗：方法：将小鼠饲养在热中性区（TNZ）内，以模拟生理反应。高密度脂蛋白胆固醇诱导肥胖相关变化，包括体重增加、内脏脂肪堆积、肌肉减少（表明肥胖性肌肉疏松症）、葡萄糖不耐受和肝甘油三酯堆积：主要结果：高热能促进肌肉中 HSP70 的表达，减轻体重增加，使 QUICK 指数正常化，并降低血浆中 HSP70 的浓度。它还降低了 HSP70 平衡的 H 指数，表明免疫炎症状态得到改善，并减少了活化的 Caspase-1 和脂肪组织中的增殖性衰老，这两者都与胰岛素抵抗有关：结论：研究结果表明，即使是 "控制 "饮食但体力活动不足的动物，在其 TNZ 范围内也会出现血糖稳态受损的情况。

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.