Lactate entrance into the brain facilities adipose tissue lipolysis during exercise via circulating calcitonin gene-related peptide.

IF 2.7 4区医学 Q3 ENDOCRINOLOGY & METABOLISM Archives of Physiology and Biochemistry Pub Date : 2024-12-01 Epub Date: 2023-11-20 DOI:10.1080/13813455.2023.2283684

Malihe Aveseh, Maryam Koushkie-Jahromi, Javad Nemati, Saeed Esmaeili-Mahani, Najmeh Sadat Hosseini

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Abstract

Objectives: We assessed the relationships between CGRP, lactate and fat regulation.

Methods: We evaluated the effect of intracerebroventricular (i.c.v.) injection of lactate and acute exercise on brain CGRP expression, and its concentration in serum/cerebrospinal fluid (SCF) in rats.

Results: Injection of lactate up-regulated CGRP expression in the cortex and CSF and activated p38-mitogen-activated protein kinases (p38-MAPK) pathway. Co-injection of lactate and sb203580, deterred lactate-induced up-regulation of CGRP in the brain and CSF. Exercise increased the CGRP expression in the brain and CSF and up-regulated fat metabolism. Inhibition of lactate entrance into the brain using alpha-cyano-4-hydroxycinnamate (4-CIN) diminished exercise-induced CGRP up-regulation in the brain and CSF. Reducing the circulating blood lactate by pre-treatment of the animals with dichloroacetate (DCA) had no effect on exercise-induced increase in CGRP expression or fat metabolism during exercise.

Conclusions: Lactate probably acts as one of a signalling molecule in the brain to regulate fat metabolism during exercise.

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运动过程中乳酸通过循环降钙素基因相关肽进入大脑，促进脂肪组织的脂解。

目的:评估CGRP、乳酸和脂肪调节之间的关系。方法:观察脑室注射乳酸和急性运动对大鼠脑CGRP表达及血清/脑脊液(SCF)中CGRP浓度的影响。结果:乳酸可上调皮质和脑脊液中CGRP的表达，激活p38-丝裂原活化蛋白激酶(p38-MAPK)通路。乳酸和sb203580联合注射可抑制乳酸诱导的脑和脑脊液CGRP上调。运动增加脑和脑脊液中CGRP的表达，上调脂肪代谢。α -氰基-4-羟基肉桂酸(4-CIN)抑制乳酸进入大脑，可减少脑和脑脊液中运动诱导的CGRP上调。用二氯乙酸(DCA)预处理降低动物循环血乳酸对运动诱导的CGRP表达和运动期间脂肪代谢的增加没有影响。结论:乳酸可能是运动过程中大脑调节脂肪代谢的信号分子之一。

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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.