Telmisartan and candesartan promote browning of white adipose tissue and reverse fatty liver changes in high fat diet fed male albino rats

Abbas, Noha A.T.; Fayed, Fawkia A.; El Sebaey, Rabab Saber; Hassan, Heba A.

doi:10.1007/s00210-023-02771-4

Cited by 1 publication

(1 citation statement)

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“…The elevated mitochondrial energy status through the Ang II/AGTR1 axis may be beneficial for the efficient consumption of blood glucose for heat production in brown adipocytes. Although angiotensin-converting enzyme inhibitors and Ang II receptor blockers are expected to prevent type 2 diabetes and obesity-associated metabolic disorders 47 , 48 , 56 , this study implies that they might affect some aspects of systemic glucose metabolism through brown adipocytes and other metabolic cells. Importantly, cold exposure potentially elevates circulating Ang II and NE levels along with the SNS activation 30 – 32 .…”

Section: Discussionmentioning

confidence: 85%

Angiotensin II participates in mitochondrial thermogenic functions via the activation of glycolysis in chemically induced human brown adipocytes

Takeda,

Yoshikawa,

Dai

2024

Sci Rep

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Brown adipocytes are potential therapeutic targets for the prevention of obesity-associated metabolic diseases because they consume circulating glucose and fatty acids for heat production. Angiotensin II (Ang II) peptide is involved in the pathogenesis of obesity- and cold-induced hypertension; however, the mechanism underlying the direct effects of Ang II on human brown adipocytes remains unclear. Our transcriptome analysis of chemical compound-induced brown adipocytes (ciBAs) showed that the Ang II type 1 receptor (AGTR1), but not AGTR2 and MAS1 receptors, was expressed. The Ang II/AGTR1 axis downregulated the expression of mitochondrial uncoupling protein 1 (UCP1). The simultaneous treatment with β-adrenergic receptor agonists and Ang II attenuated UCP1 expression, triglyceride lipolysis, and cAMP levels, although cAMP response element-binding protein (CREB) phosphorylation was enhanced by Ang II mainly through the protein kinase C pathway. Despite reduced lipolysis, both coupled and uncoupled mitochondrial respiration was enhanced in Ang II-treated ciBAs. Instead, glycolysis and glucose uptake were robustly activated upon treatment with Ang II without a comprehensive transcriptional change in glucose metabolic genes. Elevated mitochondrial energy status induced by Ang II was likely associated with UCP1 repression. Our findings suggest that the Ang II/AGTR1 axis participates in mitochondrial thermogenic functions via glycolysis.

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