How does the activation of Angiotensin II induces metabolic alteratios in adipose tisseue ans esquelituc muscle?? 

Angiotensin II (Ang II) plays a significant role in inducing metabolic alterations in adipose tissue and skeletal muscle, impacting various aspects of metabolic health. In adipose cells, Ang II inhibits insulin-stimulated insulin receptor phosphorylation, Akt activation, and glucose uptake, suggesting a pathway to insulin resistance through protein kinase C (PKC) activation. This is further supported by the observation that Ang II, through its interaction with AT1 receptors, can induce an inflammatory process mediated by the transcription factor NF-kB, contributing to the comorbidities observed in obesity, including alterations in heart, kidney, hypertension, and coagulation. Additionally, the renin-angiotensin system (RAS) activation by Ang II in adipocytes increases inflammation and endoplasmic reticulum (ER) stress, potentially through microRNAs, further linking Ang II to obesity and related diseases. Moreover, Ang II has been associated with the regulation of adipocyte glycolytic and lipolytic metabolism, indicating its role in energy metabolism within adipose tissue. Interestingly, activation of the ACE2/Ang-(1-7)/Mas axis counteracts the deleterious effects of Ang II, improving the metabolic profile and reducing fat deposition, suggesting a protective mechanism against Ang II-induced metabolic alterations. In skeletal muscle, Ang II-induced insulin resistance is suppressed by increased expression of AT1 receptor-associated protein (ATRAP), highlighting the importance of AT1 receptor hyperactivity in the development of metabolic syndrome. However, the responsiveness of peripheral tissues to Ang II in obese subjects does not significantly differ from that in non-obese subjects, suggesting a complex interaction between Ang II and metabolic alterations in obesity. Furthermore, Ang II regulates adipocyte metabolism by increasing activity and gene expression of lipogenic enzymes, mediated through insulin signaling molecules and angiotensin receptors. It directly inhibits abdominal subcutaneous adipocyte lipolysis in both normal weight and obese subjects via the AT1 receptor . Collectively, these findings illustrate the multifaceted role of Ang II in inducing metabolic alterations in adipose tissue and skeletal muscle, contributing to the pathophysiology of obesity and insulin resistance.

The relationship of angiotensin II in energy metabolism of adipocytes

Activation of Angiotensin II influences glycerol and lactate production in adipose tissue, impacting adipocyte metabolism. However, its effect on skeletal muscle metabolism is not addressed in the paper.

Angiotensin II Type 1 Receptor-associated Protein Inhibits Angiotensin II-induced Insulin Resistance with Suppression of Oxidative Stress in Skeletal Muscle Tissue

Angiotensin II activation induces insulin resistance in skeletal muscle by increasing oxidative stress and p38 MAPK activity, while adipose tissue remains unaffected, as shown in the study.

Angiotensin Converting Enzyme 2 Activator (DIZE) Modulates Metabolic Profiles in Mice, Decreasing Lipogenesis

Not addressed in the paper.

Angiotensin II Inhibits Insulin Receptor Signaling in Adipose Cells

Activation of Angiotensin II inhibits insulin signaling in adipose cells by increasing IR-Ser-phosphorylation via PKC activation, leading to impaired glucose uptake and potentially inducing insulin resistance.

Angiotensin II Increases Endoplasmic Reticulum Stress in Adipose Tissue and Adipocytes

Activation of Angiotensin II induces endoplasmic reticulum stress and inflammation in adipose tissue, contributing to obesity, possibly mediated by miRNAs and AT1 receptor, impacting metabolic alterations.

Angiotensin II and human obesity. A narrative review of the pathogenesis.

Activation of Angiotensin II induces metabolic alterations in adipose tissue and skeletal muscle through AT1 receptor interaction, triggering inflammation and contributing to obesity-related comorbidities.