1‐Sarcosine–angiotensin II infusion effects on food intake, weight loss, energy expenditure, and skeletal muscle UCP3 gene expression in a rat model

Cichello, Simon; Weisinger, R. S.; Schuijers, J.; Jois, Markandeya

doi:10.1007/s13539-014-0133-2

Cited by 12 publications

(5 citation statements)

References 35 publications

(47 reference statements)

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“…In addition, cerebral ventricular AngII infusion (50 ng/kg per min) reduces food intake, which is completely prevented by candesartan [3]. In Sprague-Dawley rats, AngII infusion impairs appetite and decreases body weight by inducing wasting predominantly in adipose tissue [15]. These findings are in accordance with the evidence showing that AT1R knockout mice are hyperphagic [16], and suggest that RAS system is directly involved in appetite regulation.…”

Section: Renin Angiotensin System Anorexia and Body Weightsupporting

confidence: 84%

Renin angiotensin system-induced muscle wasting: putative mechanisms and implications for clinicians

Afsar,

Caliskan

et al. 2024

Mol Cell Biochem

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Renin angiotensin system (RAS) alters various mechanisms related to muscle wasting. The RAS system consists of classical and non-classical pathways, which mostly function differently. Classical RAS pathway, operates through angiotensin II (AngII) and angiotensin type 1 receptors, is associated with muscle wasting and sarcopenia. On the other hand, the non-classical RAS pathway, which operates through angiotensin 1–7 and Mas receptor, is protective against sarcopenia. The classical RAS pathway might induce muscle wasting by variety of mechanisms. AngII reduces body weight, via reduction in food intake, possibly by decreasing hypothalamic expression of orexin and neuropeptide Y, insulin like growth factor-1 (IGF-1) and mammalian target of rapamycin (mTOR), signaling, AngII increases skeletal muscle proteolysis by forkhead box transcription factors (FOXO), caspase activation and muscle RING-finger protein-1 transcription. Furthermore, AngII infusion in skeletal muscle reduces phospho-Bad (Ser136) expression and induces apoptosis through increased cytochrome c release and DNA fragmentation. Additionally, Renin angiotensin system activation through AT1R and AngII stimulates tumor necrosis factor-α, and interleukin-6 which induces muscle wasting, Last but not least classical RAS pathway, induce oxidative stress, disturb mitochondrial energy metabolism, and muscle satellite cells which all lead to muscle wasting and decrease muscle regeneration. On the contrary, the non-classical RAS pathway functions oppositely to mitigate these mechanisms and protects against muscle wasting. In this review, we summarize the mechanisms of RAS-induced muscle wasting and putative implications for clinical practice. We also emphasize the areas of uncertainties and suggest potential research areas. Graphical abstract Classical and non-classical renin angiotensin systems (RAS) play opposing roles in muscle wasting. Classical RAS system operates through Angiotensin (Ang)I/ACE/AngII)/Angiotensin Type 1 Receptor (AT1R) and induces muscle wasting by mechanisms including inducing anorexia, ubiquitin–proteasome system (UPS), apoptosis, inflammation, oxidative stress, mitochondrial dysfunction, albuminuria, fibrosis (increasing transforming growth factor beta, connective tissue growth factor) and decrease insulin-like growth factor 1 (IGF-1) signaling, vitamin D and satellite cell function. Non-classical RAS system operates through Angiotensin1/ACE2/Ang (1–7)/Mas Receptor and have opposite actions to classical RAS system and protects against muscle wasting.

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Section: Renin Angiotensin System Anorexia and Body Weightsupporting

confidence: 84%

Renin angiotensin system-induced muscle wasting: putative mechanisms and implications for clinicians

Afsar,

Caliskan

et al. 2024

Mol Cell Biochem

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“…It has been reported that systemic infusion of AngII or AngII analog increases energy expenditure and reduces WAT mass in rodents. 66 , 67 However, AngII infusion is usually associated with many systemic adverse effects produced by AT1R (for example, hypertension). 66 Therefore, direct activation of AT2R by introducing exogenous selective agonists and making endogenous AngII-induced basal AT2R activity more prominent by inhibiting AT1R should be better strategies.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin type 2 receptor activation promotes browning of white adipose tissue and brown adipogenesis

Than

et al. 2017

Sig Transduct Target Ther

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Brown adipose tissue dissipates energy in the form of heat. Recent studies have shown that adult humans possess both classical brown and beige adipocytes (brown-like adipocytes in white adipose tissue, WAT), and stimulating brown and beige adipocyte formation can be a new avenue to treat obesity. Angiotensin II (AngII) is a peptide hormone that plays important roles in energy metabolism via its angiotensin type 1 or type 2 receptors (AT1R and AT2R). Adipose tissue is a major source of AngII and expresses both types of its receptors, implying the autocrine and paracrine role of AngII in regulating adipose functions and self-remodeling. Here, based on the in vitro studies on primary cultures of mouse white adipocytes, we report that, AT2R activation, either by AngII or AT2R agonist (C21), induces white adipocyte browning, by increasing PPARγ expression, at least in part, via ERK1/2, PI3kinase/Akt and AMPK signaling pathways. It is also found that AngII–AT2R enhances brown adipogenesis. In the in vivo studies on mice, administration of AT1R antagonist (ZD7155) or AT2R agonist (C21) leads to the increase of WAT browning, body temperature and serum adiponectin, as well as the decrease of WAT mass and the serum levels of TNFα, triglycerides and free fatty acids. In addition, AT2R-induced browning effect is also observed in human white adipocytes, as evidenced by the increased UCP1 expression and oxygen consumption. Finally, we provide evidence that AT2R plays important roles in hormone T3-induced white adipose browning. This study, for the first time, reveals the browning and brown adipogenic effects of AT2R and suggests a potential therapeutic target to combat obesity and related metabolic disorders.

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“…Ang II ‐induced body wasting is due to both anorexigenic and catabolic effects . Recently, Cichello et al . showed a direct effect of Ang II infusion on appetite impairment and body weight loss mostly due to adipose tissue wasting.…”

Section: Emerging Biomarkers Of Cardiac Cachexiamentioning

confidence: 99%

“…16 Ang II-induced body wasting is due to both anorexigenic and catabolic effects. 72,73 Recently, Cichello et al 74 showed a direct effect of Ang II infusion on appetite impairment and body weight loss mostly due to adipose tissue wasting. Sanders et al 75 have reported a direct catabolic effect on skeletal muscle by Ang II with increased intracellular protein degradation in murine myotubes through an increased expression of the UPP.…”

Section: Metabolic Biomarkersmentioning

confidence: 99%

Cardiac cachexia: hic et nunc

Loncar

Springer

Anker

et al. 2016

J cachexia sarcopenia muscle

113

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Cardiac cachexia (CC) is the clinical entity at the end of the chronic natural course of heart failure (HF). Despite the efforts, even the most recent definition of cardiac cachexia has been challenged, more precisely, the addition of new criteria on top of obligatory weight loss. The pathophysiology of CC is complex and multifactorial. A better understanding of pathophysiological pathways in body wasting will contribute to establish potentially novel treatment strategies. The complex biochemical network related with CC and HF pathophysiology underlines that a single biomarker cannot reflect all of the features of the disease. Biomarkers that could pick up the changes in body composition before they convey into clinical manifestations of CC would be of great importance. The development of preventive and therapeutic strategies against cachexia, sarcopenia, and wasting disorders is perceived as an urgent need by healthcare professionals. The treatment of body wasting remains an unresolved challenge to this day. As CC is a multifactorial disorder, it is unlikely that any single agent will be completely effective in treating this condition. Among all investigated therapeutic strategies, aerobic exercise training in HF patients is the most proved to counteract skeletal muscle wasting and is recommended by treatment guidelines for HF.

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1‐Sarcosine–angiotensin II infusion effects on food intake, weight loss, energy expenditure, and skeletal muscle UCP3 gene expression in a rat model

Cited by 12 publications

References 35 publications

Renin angiotensin system-induced muscle wasting: putative mechanisms and implications for clinicians

Renin angiotensin system-induced muscle wasting: putative mechanisms and implications for clinicians

Angiotensin type 2 receptor activation promotes browning of white adipose tissue and brown adipogenesis

Cardiac cachexia: hic et nunc

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