Journal of Endocrinology最新文献

The effects of GIP, GLP-1 and GLP-2 on markers of bone turnover: a review of the gut-bone axis.

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2025-03-01 DOI: 10.1530/JOE-24-0231

Miriam Longo, David Siersbaek Mathiesen, Laerke Gasberg, Katherine Esposito, Asger Bach Lund, Filip K Knop

{"title":"The effects of GIP, GLP-1 and GLP-2 on markers of bone turnover: a review of the gut-bone axis.","authors":"Miriam Longo, David Siersbaek Mathiesen, Laerke Gasberg, Katherine Esposito, Asger Bach Lund, Filip K Knop","doi":"10.1530/JOE-24-0231","DOIUrl":"10.1530/JOE-24-0231","url":null,"abstract":"Bone is a dynamic tissue continuously undergoing remodelling processes of resorption and formation to maintain bone mass and health. Food intake and the release of the gut-derived incretin hormones including glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) as well as its 'sister hormone' glucagon-like peptide 2 (GLP-2), appear to regulate bone turnover processes in the postprandial state as part of the so-called gut-bone axis. The effects of these gut hormones on bone metabolism depend on their circulating concentrations. While at physiological concentrations, elicited by nutrient intake, GIP seems to be the main contributor to postprandial bone resorption, supraphysiological concentrations of gut hormones induce more potent and robust anti-resorptive effects. This review provides an overview of the literature describing the role of gut-derived hormones in the regulation and maintenance of bone tissue. Also, we describe the effects of gut hormone-based treatment modalities on bone health and discuss the potential of gut hormone-based strategies for the treatment of bone disorders in the future.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Glucose and energy metabolism are impaired in mice deficient for orexins.

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2025-03-01 DOI: 10.1530/JOE-24-0329

Mélodie Devère, Saloua Takhlidjt, David Godefroy, Jean Luc do Rego, Jean-Claude Do Rego, Alexandre Benani, Emmanuelle Nedelec, Nicolas Chartrel, Marie Picot

{"title":"Glucose and energy metabolism are impaired in mice deficient for orexins.","authors":"Mélodie Devère, Saloua Takhlidjt, David Godefroy, Jean Luc do Rego, Jean-Claude Do Rego, Alexandre Benani, Emmanuelle Nedelec, Nicolas Chartrel, Marie Picot","doi":"10.1530/JOE-24-0329","DOIUrl":"10.1530/JOE-24-0329","url":null,"abstract":"The present study aims to investigate the impact of orexin deficiency on the regulation of energy and glucose metabolism using a mouse model depleted for the prepro-orexin gene. Our data reveal that, despite a decrease of food consumption (at least in males), orexin deficiency induces a significant increase in body weight that is associated with an alteration of the body composition, as males and females orexin deficient mice display an increased fat mass compared to the wild-type littermates. Nevertheless, no significant differences of global energy expenditure and locomotor activity were observed in the mutant mice relative to the control. Glucose homeostasis is also impaired in the absence of orexins, since glucose tolerance and insulin secretion are diminished, and insulin sensitivity is slightly reduced. In addition, the livers of the male orexin-KO mice are significantly larger and heavier with more adipose tissue than the wild type mice. Interestingly, orexin-deficient mice present an upregulation of liver enzyme involved in gluconeogenesis and a down-regulation of GCK, an enzyme which promotes glycogen storage, that may participate to the altered glucose metabolism of the orexin mutant mice. To conclude, the present study indicates that orexin deficiency induces profound alteration in the regulation of energy and glucose metabolism, which is more pronounced in males than in females. These findings support the idea that dysfunction of this orexin system may promote obesity and diabetes, and could represent an interesting therapeutic target in the context of 'diabesity'.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reappraising the relationship between hyperinsulinemia and insulin resistance in PCOS.

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2025-02-01 DOI: 10.1530/JOE-24-0269

Emma Jane Houston, Nicole Meredith Templeman

{"title":"Reappraising the relationship between hyperinsulinemia and insulin resistance in PCOS.","authors":"Emma Jane Houston, Nicole Meredith Templeman","doi":"10.1530/JOE-24-0269","DOIUrl":"10.1530/JOE-24-0269","url":null,"abstract":"Polycystic ovary syndrome (PCOS), a reproductive endocrine disorder with quintessential features of metabolic dysfunction, affects millions of women worldwide. Hyperinsulinemia (i.e., elevated insulin without hypoglycemia) is a common metabolic feature of PCOS that worsens its reproductive symptoms by exacerbating pituitary hormone imbalances and increasing levels of bioactive androgens. Hyperinsulinemia in PCOS is often attributed to insulin resistance, based on the concept that impaired insulin-mediated glucose disposal would induce compensatory insulin hypersecretion. However, it is challenging to define the sequential relationship between insulin sensitivity and insulin secretion, as they are tightly interlinked, and evidence suggests that hyperinsulinemia can alternatively precede insulin resistance. Notably, other drivers of hyperinsulinemia (outside of insulin resistance) may be highly relevant in the context of PCOS. For instance, high androgen levels can augment both hyperinsulinemia and insulin resistance, generating a self-perpetuating cycle of reproductive and metabolic dysfunction. In this review, we evaluate the cause-and-effect relationships between insulin resistance and hyperinsulinemia in PCOS. We examine evidence for the prevailing theory of insulin resistance as the primary defect that causes secondary compensatory hyperinsulinemia, and an alternative framework of hyperinsulinemia as the earlier defect that perpetuates reproductive and metabolic features of PCOS. Considering the heterogenous nature of PCOS, it is improbable that its metabolic characteristics always follow the same progression. Comprehensively examining all mechanistic regulators of hyperinsulinemia and insulin resistance in PCOS might thereby lead to improved prevention and management strategies, and address critical knowledge gaps in the progression of PCOS pathogenesis.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11906131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143515865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

GLP-1R/NPY2R regulate gene expression, ovarian and adrenal morphology in HFD mice. GLP-1R/NPY2R调节HFD小鼠的基因表达、卵巢和肾上腺形态。

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2025-01-10 Print Date: 2025-02-01 DOI: 10.1530/JOE-24-0189

Dawood Khan, Ananyaa Sridhar, Charlotte R Moffett

{"title":"GLP-1R/NPY2R regulate gene expression, ovarian and adrenal morphology in HFD mice.","authors":"Dawood Khan, Ananyaa Sridhar, Charlotte R Moffett","doi":"10.1530/JOE-24-0189","DOIUrl":"10.1530/JOE-24-0189","url":null,"abstract":"Glucagon-like peptide-1 receptor (GLP-1R) and neuropeptide Y receptors (NPYRs) are expressed in reproductive tissues contributing to the regulation of gonadal function. This exploratory study examines the potential impact of their modulation by assessing the effects of exendin-4 (Ex-4) and peptide YY (PYY) (3-36) on endocrine ovaries and adrenals in high-fat diet (HFD) mice. Ex-4 and PYY(3-36) reduced blood glucose and energy intake, with no effects on body weight. While HFD did not impact the estrous cycle, Ex-4 increased metestrus frequency and decreased diestrus frequency resulting in 0% mice experiencing repeated diestrus or becoming acyclic. Luteinizing hormone levels were significantly higher in the Ex-4 and PYY(3-36) groups compared to the normal diet and HFD controls. In the adrenals, reduced capsule and zona glomerulosa thickness caused by HFD was reversed after peptide treatments. Within the ovaries, HFD increased the number of atretic follicles, an effect that disappeared after Ex-4 and PYY(3-36) treatments. Ex-4 also increased the number of corpora lutea owing to the prolonged metestrus phase. Gene expression analysis within the adrenals revealed the upregulation of Insr and the downregulation of Prgtr in HFD mice, while Ex-4 downregulated the expression of Gipr. The ovarian gene expression of Gipr, Npy1r and Prgtr was downregulated by Ex-4 treatment, while PYY(3-36) significantly downregulated the Prgtr expression compared to HFD mice. These data indicate that manipulating GLP-1R and NPY2R leads to changes in the reproductive physiology of mice. In addition, the observed alterations in the morphology and gene expression in the adrenals and ovaries imply a direct impact of these peptides on female reproductive function.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11798413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Continuing the success of Journal of Endocrinology and Journal of Molecular Endocrinology: Editor-in-Chief handover. 延续《内分泌学杂志》和《分子内分泌学杂志》的成功：主编交接。

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2024-12-18 Print Date: 2025-01-01 DOI: 10.1530/JOE-24-0305

Martin Haluzik, Gabriela da Silva Xavier

引用次数: 0

Glucocorticoid excess alters metabolic rate and substrate utilisation via 11β-HSD1. 糖皮质激素过量会通过 11β-HSD1 改变代谢率和底物利用率。

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2024-10-28 Print Date: 2024-11-01 DOI: 10.1530/JOE-24-0205

Samuel R Heaselgrave, Silke Heising, Stuart A Morgan, David M Carthwright, Michael Sagmeister, Rowan S Hardy, Craig L Doig, Nicholas Morton, Kostas Tsintzas, Gareth G Lavery

{"title":"Glucocorticoid excess alters metabolic rate and substrate utilisation via 11β-HSD1.","authors":"Samuel R Heaselgrave, Silke Heising, Stuart A Morgan, David M Carthwright, Michael Sagmeister, Rowan S Hardy, Craig L Doig, Nicholas Morton, Kostas Tsintzas, Gareth G Lavery","doi":"10.1530/JOE-24-0205","DOIUrl":"10.1530/JOE-24-0205","url":null,"abstract":"Systemic glucocorticoid excess causes several adverse metabolic conditions, most notably Cushing's syndrome. These effects are amplified by the intracellular enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Here, we determined the less well-characterised effects of glucocorticoid excess, and the contribution of 11β-HSD1 amplification on metabolic rate in mice. Male and female C57BL/6J (wild type, WT) and 11β-HSD1 knockout (11β-HSD1 KO) mice were treated with high-dose corticosterone or a vehicle control for 3 weeks. Indirect calorimetry was conducted during the final week of treatment, with or without fasting, to determine the impact on metabolic rate. We found that corticosterone treatment elevated metabolic rate and promoted carbohydrate utilisation primarily in female WT mice, with effects more pronounced during the light phase. Corticosterone treatment also resulted in greater fat accumulation in female WT mice. Corticosterone induced hyperphagia was identified as a likely causal factor altering the respiratory exchange ratio (RER) but not energy expenditure (EE). Male and female 11β-HSD1 KO mice were protected against these effects. We identify novel metabolic consequences of sustained glucocorticoid excess, identify a key mechanism of hyperphagia, and demonstrate that 11β-HSD1 is required to manifest the full metabolic derangement.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11558800/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

GLP-1 receptor agonist-based therapies and cardiovascular risk: a review of mechanisms. GLP-1 受体激动剂与心血管风险：机制综述。

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2024-09-19 Print Date: 2024-10-01 DOI: 10.1530/JOE-24-0046

Neerav Mullur, Arianne Morissette, Nadya M Morrow, Erin E Mulvihill

{"title":"GLP-1 receptor agonist-based therapies and cardiovascular risk: a review of mechanisms.","authors":"Neerav Mullur, Arianne Morissette, Nadya M Morrow, Erin E Mulvihill","doi":"10.1530/JOE-24-0046","DOIUrl":"10.1530/JOE-24-0046","url":null,"abstract":"Cardiovascular outcome trials (CVOTs) in people living with type 2 diabetes mellitus and obesity have confirmed the cardiovascular benefits of glucagon-like peptide 1 receptor agonists (GLP-1RAs), including reduced cardiovascular mortality, lower rates of myocardial infarction, and lower rates of stroke. The cardiovascular benefits observed following GLP-1RA treatment could be secondary to improvements in glycemia, blood pressure, postprandial lipidemia, and inflammation. Yet, the GLP-1R is also expressed in the heart and vasculature, suggesting that GLP-1R agonism may impact the cardiovascular system. The emergence of GLP-1RAs combined with glucose-dependent insulinotropic polypeptide and glucagon receptor agonists has shown promising results as new weight loss medications. Dual-agonist and tri-agonist therapies have demonstrated superior outcomes in weight loss, lowered blood sugar and lipid levels, restoration of tissue function, and enhancement of overall substrate metabolism compared to using GLP-1R agonists alone. However, the precise mechanisms underlying their cardiovascular benefits remain to be fully elucidated. This review aims to summarize the findings from CVOTs of GLP-1RAs, explore the latest data on dual and tri-agonist therapies, and delve into potential mechanisms contributing to their cardioprotective effects. It also addresses current gaps in understanding and areas for further research.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11466209/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141982464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Aldosterone, mitochondria and regulation of cardiovascular metabolic disease. 醛固酮、线粒体和心血管代谢疾病的调节。

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2024-09-13 Print Date: 2024-10-01 DOI: 10.1530/JOE-23-0350

Cheng-Hsuan Tsai, Zheng-Wei Chen, Bo-Ching Lee, Che-Wei Liao, Yi-Yao Chang, Yan-Rou Tsai, Chia-Hung Chou, Vin-Cent Wu, Chi-Sheng Hung, Yen-Hung Lin

{"title":"Aldosterone, mitochondria and regulation of cardiovascular metabolic disease.","authors":"Cheng-Hsuan Tsai, Zheng-Wei Chen, Bo-Ching Lee, Che-Wei Liao, Yi-Yao Chang, Yan-Rou Tsai, Chia-Hung Chou, Vin-Cent Wu, Chi-Sheng Hung, Yen-Hung Lin","doi":"10.1530/JOE-23-0350","DOIUrl":"10.1530/JOE-23-0350","url":null,"abstract":"Aldosterone is a mineralocorticoid hormone involved in controlling electrolyte balance, blood pressure, and cellular signaling. It plays a pivotal role in cardiovascular and metabolic physiology. Excess aldosterone activates mineralocorticoid receptors, leading to subsequent inflammatory responses, increased oxidative stress, and tissue remodeling. Various mechanisms have been reported to link aldosterone with cardiovascular and metabolic diseases. However, mitochondria, responsible for energy generation through oxidative phosphorylation, have received less attention regarding their potential role in aldosterone-related pathogenesis. Excess aldosterone leads to mitochondrial dysfunction, and this may play a role in the development of cardiovascular and metabolic diseases. Aldosterone has the potential to affect mitochondrial structure, function, and dynamic processes, such as mitochondrial fusion and fission. In addition, aldosterone has been associated with the suppression of mitochondrial DNA, mitochondria-specific proteins, and ATP production in the myocardium through mineralocorticoid receptor, nicotinamide adenine dinucleotide phosphate oxidase, and reactive oxygen species pathways. In this review, we explore the mechanisms underlying aldosterone-induced cardiovascular and metabolic mitochondrial dysfunction, including mineralocorticoid receptor activation and subsequent inflammatory responses, as well as increased oxidative stress. Furthermore, we review potential therapeutic targets aimed at restoring mitochondrial function in the context of aldosterone-associated pathologies. Understanding these mechanisms is vital, as it offers insights into novel therapeutic strategies to mitigate the impact of aldosterone-induced mitochondrial dysfunction, thereby potentially improving the outcomes of individuals affected by cardiovascular and metabolic disorders.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141909808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The GHSR1a antagonist LEAP2 regulates islet hormone release in a sex-specific manner GHSR1a 拮抗剂 LEAP2 以性别特异性方式调节胰岛激素的释放

IF 4 3区医学

Journal of Endocrinology Pub Date : 2024-09-01 DOI: 10.1530/joe-24-0135

Nirun Hewawasam, Debalina Sakar, Olivia Bolton, Blerinda Delishaj, Maha Almutairi, Aileen King, Ayse S Dereli, Chloe Despontin, Patrick Gilon, Sue Reeves, Michael Patterson, Astrid Christine Hauge-Evans

{"title":"The GHSR1a antagonist LEAP2 regulates islet hormone release in a sex-specific manner","authors":"Nirun Hewawasam, Debalina Sakar, Olivia Bolton, Blerinda Delishaj, Maha Almutairi, Aileen King, Ayse S Dereli, Chloe Despontin, Patrick Gilon, Sue Reeves, Michael Patterson, Astrid Christine Hauge-Evans","doi":"10.1530/joe-24-0135","DOIUrl":"https://doi.org/10.1530/joe-24-0135","url":null,"abstract":"LEAP2, a liver-derived antagonist for the ghrelin receptor, GHSR1a, counteracts effects of ghrelin on appetite and energy balance. Less is known about its impact on blood glucose-regulating hormones from pancreatic islets. Here we investigate whether acyl-ghrelin (AG) and LEAP2 regulate islet hormone release in a cell type- and sex-specific manner. Hormone content from secretion experiments with isolated islets from male and female mice was measured by radioimmunoassay and mRNA expression by qPCR. LEAP2 enhanced insulin secretion in islets from males (p<0.01) but not females (p<0.2), whilst AG-stimulated somatostatin release was significantly reversed by LEAP2 in males (p<0.001) but not females (p<0.2). Glucagon release was not significantly affected by AG and LEAP2. Ghsr1a, Ghrelin, Leap2, Mrap2, Mboat4 and Sstr3 islet mRNA expression did not differ between sexes. In control male islets maintained without 17-beta oestradiol (E2), AG exerted an insulinostatic effect (p<0.05), with a trend towards reversal by LEAP2 (p=0.06). Both were abolished by 72h E2 pre-treatment (10 nmol/l, p<0.2). AG-stimulated somatostatin release was inhibited by LEAP2 from control (p<0.001) but not E2-treated islets (p<0.2). LEAP2 and AG did not modulate insulin secretion from MIN6 beta cells and Mrap2 was downregulated (P<0.05) and Ghsr1a upregulated (P<0.0001) in islets from Sst-/-\u0000 mice. Our findings show that AG and LEAP2 regulate insulin and somatostatin release in an opposing and sex-dependent manner, which in males can be modulated by E2. We suggest that regulation of SST release is a key starting point for understanding the role of GHSR1a in islet function and glucose metabolism.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":"31 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142255678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The mineralocorticoid system, cardiometabolic health and its interplay with adipose tissue 矿皮质激素系统、心脏代谢健康及其与脂肪组织的相互作用

IF 4 3区医学

Journal of Endocrinology Pub Date : 2024-09-01 DOI: 10.1530/joe-24-0119

Moe Thuzar, Muthanna Abdul Halim, Michael Stowasser

{"title":"The mineralocorticoid system, cardiometabolic health and its interplay with adipose tissue","authors":"Moe Thuzar, Muthanna Abdul Halim, Michael Stowasser","doi":"10.1530/joe-24-0119","DOIUrl":"https://doi.org/10.1530/joe-24-0119","url":null,"abstract":"The mineralocorticoid system, comprising the renin-angiotensin-aldosterone system (RAAS) and associated receptors, is traditionally viewed as a regulator of sodium and fluid balance and blood pressure (BP), with the main mineralocorticoid hormone aldosterone acting via the mineralocorticoid receptor (MR) in distal renal tubules. Over the past few decades, there has been a wider understanding of the role of the mineralocorticoid system in regulating both classical BP-dependent and non-BP-dependent systemic effects. Mounting evidence indicates the novel role of the mineralocorticoid system in cardiometabolic health with excess mineralocorticoid system activity being associated with adiposity, diabetes, insulin resistance and cardiovascular diseases independent of its effect on BP, and RAAS blockade and MR antagonists offering protection against cardiometabolic dysfunction. The metabolic manifestations of mineralocorticoid system overactivation are mainly mediated by their interactions with adipose tissue which orchestrates energy, lipids and glucose homeostasis via effects on the functions of brown and white adipocytes and immune cells. Adipose tissue can in turn influence mineralocorticoid system activity by harbouring its own RAAS system and by releasing mineralocorticoid-secretory factors/adipokines, with resultant further progression of cardiometabolic dysfunction. This article discusses the interplay between the mineralocorticoid system and adipose tissue in the pathophysiology of cardiometabolic diseases.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":"102 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142255676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0