Reviews in Endocrine & Metabolic Disorders最新文献

{"title":"Association between metabolic dysfunction-associated steatotic liver disease/non-alcoholic fatty liver disease and chronic kidney disease: a systematic review and meta-analysis.","authors":"André O Soares, Davi A C Loli, Gustavo R Carvalho, Vinicius Daher Alvares Delfino, Paulo Roberto Bignardi","doi":"10.1007/s11154-026-10059-0","DOIUrl":"10.1007/s11154-026-10059-0","url":null,"abstract":"<p><p>Data from current literature have suggested a positive association between Steatotic Liver Disease (SLD) and Chronic Kidney Disease (CKD). In 2023, a consensus of experts suggested that the term metabolic associated steatotic liver disease (MASLD) be used instead of non-alcoholic fatty liver disease (NAFLD), a term that had long been used to indicate the situation of hepatic steatosis not related to alcohol consumption or secondary to another etiology. The majority of hepatologists accepted this suggestion. To critically analyze this described association and compare the impact of change in criteria, we performed a systematic review followed by meta-analysis of incidence studies that evaluated the occurrence of new cases of CKD in patients diagnosed with NAFLD and MAFLD/MASLD. We searched the PubMed, LILACS, SciELO, and Cochrane Library databases for longitudinal studies published through June 2025 that included groups with NAFLD, MAFLD, and/or MASLD, as well as a control group, in the adult population without CKD at baseline. Among 2,099 studies found, twenty met the inclusion criteria. Compared to the patient's control group, the risk ratio (RR) for incidence of CKD in the group with MAFLD, MASLD, and NAFLD was 1.29 (1.18-1.40), 1.16 (1.12-1.19) and 1.25 (1.14-1.36), respectively. In a new analysis grouping MASLD with MAFLD to assess the impact of the terminology shift, the results remained similar. This review demonstrates that SLD is associated with the risk of developing CKD, regardless of classification. However, this connection needs further elucidation of its mechanisms to comprehend it better and prevent its impact.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":"999-1021"},"PeriodicalIF":8.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13616005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148219480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling the role of aldosterone in metabolic dysfunction-associated steatotic liver disease.","authors":"Anna Hernández-Rubio, Maria-Teresa Julián, Elena Valassi, Nuria Alonso, Manel Puig-Domingo","doi":"10.1007/s11154-026-10056-3","DOIUrl":"10.1007/s11154-026-10056-3","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is an increasing global health challenge closely linked to obesity and the metabolic syndrome. This review explores the role of aldosterone as a central contributor to metabolic dysfunction, highlighting its association with adipose tissue dysfunction and systemic insulin resistance which can further influence MASLD development and progression. While aldosterone-related organ damage has been extensively studied in other contexts such as kidney disease, its involvement in MASLD has received less attention. Beyond classical renin-angiotensin-aldosterone system activation, aldosterone secretion can be directly stimulated by leptin and other adipogenic factors, creating a pathogenic link between obesity and metabolic impairment. Aldosterone amplifies chronic inflammation, oxidative stress and insulin resistance, primarily through mineralocorticoid receptor (MR)-dependent mechanisms. These involve both genomic actions regulating pro-inflammatory genes and rapid non-genomic signalling. Additionally, aldosterone MR-independent effects, can further contribute to oxidative stress and inflammatory responses. Significantly, the MR is expressed in liver cells, including hepatocytes, liver sinusoidal endothelial cells, Kupffer cells, and hepatic stellate cells. This expression can allow for direct aldosterone-mediated effect on hepatic inflammation, oxidative stress, and fibrosis, which can occur alongside or independently of systemic metabolic pathways. Such direct mechanisms may explain associations found in clinical studies correlating high aldosterone levels -even with low renin- with the prevalence and progression of MASLD. Recognizing aldosterone as a pleiotropic hormone that integrates metabolic and hepatic disease offers new insights into the cardio-kidney-metabolic syndrome and underscores the potential for targeted therapies.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":"943-958"},"PeriodicalIF":8.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13616020/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148353299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An elusive link between blood measures of advanced glycation end products and their receptors and cognitive impairment syndromes in people with diabetes: A scoping review.","authors":"Allison L B Shapiro, Nopporn Thangthaeng, Kristen DeSanto, Brianne M Bettcher, Anthony A Killeen","doi":"10.1007/s11154-026-10061-6","DOIUrl":"10.1007/s11154-026-10061-6","url":null,"abstract":"<p><p>Advanced glycation end products (AGEs), which are glycated forms of proteins and lipids, are increased in diabetes resulting from chronic hyperglycemia. AGEs and their receptor (RAGE) have been linked to cognitive impairment syndromes and may increase the risk of cognitive decline and impairment in people with diabetes who experience chronic hyperglycemia. The objective of this scoping review was to comprehensively document the current evidence concerning the relationship between AGEs and RAGE, measured in the blood, and cognitive function and cognitive impairment syndromes in people with diabetes. MEDLINE, Embase, Cochrane Library, Web of Science Core Collection, APA PsycInfo, and the Psychology and Behavioral Sciences Collection were queried, and the PRISMA Extension for Scoping Reviews guidelines were followed for reporting of methods and results. Twenty-two articles were included in the current scoping review. Among the included articles, we found largely mixed results, whereby both higher and lower levels of AGEs/RAGE were associated with worse cognition or presence of cognitive impairment syndromes in people with diabetes; however, due to notable differences in the methodologies employed to quantify AGEs/RAGE in blood, it is challenging to interpret the factors driving the observed variability. Methodological differences that are likely relevant to AGEs/RAGE quantification include use of plasma vs. serum and selection of AGEs/RAGE studied (e.g., total AGEs/RAGE, pentosidine, carboxymethyl lysine, etc.). Given the observed inconsistencies, currently, there is insufficient evidence to conclude that blood-based AGEs and/or RAGE are indicators of risk for cognitive impairment and decline in people with diabetes. Moreover, it remains undetermined as to which AGEs species or RAGE isoform is most predictive of cognitive impairment or decline in people with diabetes. More studies are needed that include larger sample sizes and well-described and validated methodology to measure AGEs/RAGE.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":"977-998"},"PeriodicalIF":8.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148272647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of the impact of oxidative stress and inflammation on placental angiogenesis in women with gestational diabetes mellitus (GDM).","authors":"Angelika Buczyńska-Backiel, Maria Kościuszko, Adam Jacek Krętowski, Małgorzata Szelachowska","doi":"10.1007/s11154-026-10060-7","DOIUrl":"10.1007/s11154-026-10060-7","url":null,"abstract":"<p><p>Gestational diabetes mellitus (GDM) is defined by maternal hyperglycemia, yet growing evidence indicates that it is a systemic disorder involving oxidative stress, inflammation, endothelial dysfunction and altered placental angiogenesis. The placenta plays a central role in translating maternal metabolic disturbances into fetal and vascular consequences. This narrative review aimed to synthesize current experimental and clinical evidence on the role of oxidative stress and inflammation in the regulation of placental angiogenesis in GDM. The reviewed studies consistently demonstrate that pregnancies complicated by GDM are characterized by increased oxidative stress and inflammatory activity at both systemic and placental levels. These disturbances are associated with endothelial dysfunction and dysregulation of angiogenic signaling, leading to abnormal placental vascular remodeling. Genetic susceptibility primarily influences maternal glucose metabolism, while placental oxidative and angiogenic alterations appear to develop downstream of metabolic stress and are further modulated by epigenetic mechanisms. Collectively, these processes contribute to the characteristic placental phenotype of GDM and may underlie fetal programming and long-term cardiometabolic risk in the offspring. Importantly, evidence from randomized trials and meta-analyses indicates that antioxidant-oriented interventions can partially improve redox balance, inflammatory status, and metabolic indices in women with GDM. Current evidence suggests that oxidative stress may represent a central link between maternal hyperglycemia and placental vascular dysfunction in GDM. Beyond glycemic control, targeting redox imbalance and inflammatory pathways may represent a potential complementary strategy to improve placental function and pregnancy outcomes. Integration of oxidative, inflammatory, and angiogenic biomarkers into future longitudinal studies may facilitate biological stratification of GDM and support the development of more personalized therapeutic approaches.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":"959-976"},"PeriodicalIF":8.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13616002/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148164228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Natriuretic peptide receptor C in cardiovascular-kidney-liver-metabolic syndrome: from natriuretic peptide deficiency to direct tissue signaling?","authors":"Matteo Landolfo, Francesco Spannella, Chiara Salvà, Bernhard Radlinger, Susanne Kaser, Alessandro Gezzi, Riccardo Sarzani","doi":"10.1007/s11154-026-10066-1","DOIUrl":"10.1007/s11154-026-10066-1","url":null,"abstract":"<p><p>The cardiovascular-renal-liver-metabolic (CKLM) syndrome integrates dysmetabolically driven heart, vascular, kidney, and liver diseases through a shared pathophysiological substrate. In obesity, upregulation of the clearance natriuretic peptide receptor C (NPR-C) in adipose tissue creates a \"NP deficiency,\" undermining the protective cardiovascular and metabolic actions of endogenous NPs. Recent preclinical data demonstrates that NPR-C functions beyond simple peptide clearance. Through interactions with ligands like CNP, musclin, and osteocrin, NPR-C triggers context-dependent intracellular signaling. In experimental models, independent of systemic NP levels, NPR-C directly modulates cardiac remodeling, podocyte injury, hepatic steatosis, vascular inflammation, and adipocyte function. This review synthesizes NPR-C biology within the CKLM framework. While human validation remains limited, targeting tissue-specific NPR-C pathways represents a promising therapeutic frontier for restoring cardiometabolic homeostasis.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":"1091-1107"},"PeriodicalIF":8.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13616004/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148423769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional pituitary adenoma imaging.","authors":"Linus Hesse, Linus Haberbosch","doi":"10.1007/s11154-026-10063-4","DOIUrl":"10.1007/s11154-026-10063-4","url":null,"abstract":"<p><p>High-resolution pituitary MRI localises most pituitary neuroendocrine tumours (PitNETs), yet clinically important subgroups remain challenging: (i) very small functioning tumours, particularly corticotroph microadenomas, and (ii) post-operative remnants where scar, gland and tumour cannot be reliably separated. Functional imaging, specifically PET has matured into a problem-solving modality when conventional imaging is equivocal, provided it is used selectively and interpreted within a physiology-led framework. This review proposes an MRI-first, tiered imaging strategy and a pragmatic approach to tracer selection from the available armamentarium ([¹¹C]methionine, [⁶⁸ Ga]SSTR ligands, [⁶⁸ Ga]PentixaFor, [¹⁸F]FET and [¹⁸F]FDG). We emphasise how to optimise PET acquisition and reporting, and how to integrate imaging with endocrine phenotype, treatment history and surgical/radiosurgical planning to maximise clinical impact while safeguarding pituitary function.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":"1059-1076"},"PeriodicalIF":8.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13616001/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148265783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Where are we in the diagnosis and treatment of hirsutism? A narrative review.","authors":"Mert Yesiladali, Kursad Unluhizarci, Erkut Attar, Fahrettin Kelestimur","doi":"10.1007/s11154-026-10057-2","DOIUrl":"10.1007/s11154-026-10057-2","url":null,"abstract":"<p><strong>Background: </strong>Hirsutism is a prevalent androgen-dependent condition that significantly affects women's physical and psychological health. Despite decades of study, major gaps persist in understanding local androgen metabolism, the role of insulin resistance, and individualized treatment responses. This review aims to provide a contemporary update that integrates recent molecular, diagnostic, and therapeutic advances.</p><p><strong>Objective: </strong>To critically appraise the current understanding of hirsutism, with an emphasis on: (1) emerging concepts in local androgen action and follicular sensitivity, (2) evolving assessment methods, (3) updated pharmacologic and mechanical treatment options aligned with current endocrine and dermatologic evidence.</p><p><strong>Search methods: </strong>A narrative review of the literature was conducted in PubMed, Scopus, and Web of Science for studies published between January 2000 and September 2025, using the terms: \"hirsutism,\" \"hyperandrogenism,\" \"androgen excess,\" \"idiopathic hirsutism,\" \"PCOS,\" \"5α-reductase,\" \"antiandrogens,\" \"oral contraceptives,\" \"laser hair removal,\" and \"insulin resistance.\"</p><p><strong>Inclusion criteria: </strong>human studies, English language, adult females, and peer-reviewed original or review articles.</p><p><strong>Wider implications: </strong>An integrated understanding of systemic and local androgenic activity is transforming the management of hirsutism from a purely cosmetic issue to a complex endocrine disorder with metabolic and psychological dimensions. This review proposes a personalized, multidisciplinary framework that bridges endocrinology, gynecology, and dermatology. Future directions should focus on elucidating local androgen metabolism, tissue-specific enzyme activity, and the role of insulin resistance in idiopathic cases to refine both diagnostic precision and treatment efficacy.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":"1041-1057"},"PeriodicalIF":8.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13615992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148151047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond metabolic control: the potential role of antidiabetic therapies in modulating male reproductive function and spermatogenesis.","authors":"Valentina Paternò, Roberto Abdel Malek, Enrico Delli Paoli, Anna Chiara Conflitti, Ernesto Maddaloni, Costanzo Gabriele, Tommaso Piticchio, Rosario Le Moli, Giulio Geraci, Raffaella Buzzetti, Francesco Lombardo, Donatella Paoli, Francesco Pallotti","doi":"10.1007/s11154-026-10090-1","DOIUrl":"https://doi.org/10.1007/s11154-026-10090-1","url":null,"abstract":"<p><p>In recent years, novel antidiabetic drugs, particularly sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1 RA), have attracted increasing interest for their effects beyond glycemic control, including potential actions on male reproductive function. This review critically summarizes current evidence regarding the impact of antidiabetic therapies on spermatogenesis, testicular metabolic homeostasis, and male gonadal function, focusing on the underlying molecular and pathophysiological mechanisms. Experimental evidence suggests that metabolic dysfunction, oxidative stress, inflammation, apoptosis, and impaired Sertoli cell metabolism play a central role in diabetes- and obesity-associated male reproductive dysfunction. In this context, SGLT2i and GLP-1 RA appear capable of modulating several of these pathways, improving sperm parameters, preserving testicular architecture, and attenuating oxidative and inflammatory damage in preclinical models. Emerging data also suggest possible direct gonadal effects mediated through intracellular signaling pathways involved in steroidogenesis, autophagy, and cellular energy regulation. However, clinical evidence remains limited and partly conflicting, and it is still unclear whether these findings translate into clinically meaningful reproductive benefits in humans. Preliminary evidence suggests that dual GIP/GLP-1 receptor agonists, such as tirzepatide, may exert beneficial effects on male reproductive health. However, direct evidence regarding their impact on spermatogenesis and fertility remains limited. Overall, well-designed prospective clinical studies incorporating reproductive and hormonal outcomes are warranted to better define the role of these therapies within an integrated andro-metabolic approach to the management of obesity- and diabetes-associated male reproductive dysfunction.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149114300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Shared and distinct genetic architectures of eating disorders and obesity: From monogenic causes to polygenic risk.","authors":"Luisa Sophie Rajcsanyi, Triinu Peters, Anke Hinney","doi":"10.1007/s11154-026-10088-9","DOIUrl":"https://doi.org/10.1007/s11154-026-10088-9","url":null,"abstract":"<p><p>Eating disorders and obesity are severe health conditions arising from an impaired body weight regulation. Both are strongly influenced by genetic factors. Accordingly, obesity can be broadly classified as either monogenic, caused by mutations in a single gene, or polygenic, resulting from the cumulative effects of numerous variants, each exerting modest effects on body weight. Although the genetic architecture of obesity is relatively well characterized, novel mutations underlying monogenic obesity are still being uncovered, and the mechanisms linking polygenic variants to the phenotype are not fully elucidated. In contrast, the genetic basis of eating disorders is considerably less well understood. Among these, anorexia nervosa has been the most intensively studied, with several genomic regions already associated with disease susceptibility. The present review summarizes the current knowledge about the genetics of obesity and anorexia nervosa, highlighting shared and distinct mechanisms and discusses emerging research directions.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149114318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Levothyroxine monotherapy has limited effects on body composition in clinical and subclinical hypothyroidism: a systematic review and meta-analysis.","authors":"Derrick Kretli-Souza, Gabriel Meireles-Oliveira, Raiane Aparecida Asevedo, Nathalia Elizabete Paulino, Yuri Alves-Silva, Ingrid Rodrigues Hortêncio-Medeiros, Dayani Silvina de Jesus, Sara Cristina Leonel Lemos, Candido Celso Coimbra, Lucas Rios Drummond, Helton Oliveira Campos, Rodrigo Antonio Peliciari-Garcia, Paula Bargi-Souza","doi":"10.1007/s11154-026-10093-y","DOIUrl":"https://doi.org/10.1007/s11154-026-10093-y","url":null,"abstract":"<p><p>Clinical (CH) and subclinical (SCH) hypothyroidism reduces the metabolic rate and alter body composition. The current treatment with levothyroxine (LT4) restores the thyroid axis hormonal levels; however, its efficacy in reversing the anthropometric alterations remains unclear. This review was prospectively registered on PROSPERO (CRD42024589156), followed PRISMA guidelines, and aimed to include studies involving CH and/or SCH treated with LT4 monotherapy until achieving physiological hormonal levels. Eligible studies reported pre- and post-LT4 treatment data of BMI, BW, fat mass (FM), and lean mass/fat-free mass (LM/FFM). Each variable was analyzed according to treatment duration, sex distribution, initial and final TSH levels. 35 studies were included, comprising 1,116 individuals with hypothyroidism (672 CH; 444 SCH). In CH, LT4 led to negligible changes in BMI in the general analysis (Standardized mean difference [SMD] -0.18; 95% confidence interval [CI] -0.26, -0.10; mean difference [MD] -0.68 kg/m²), while moderate BMI reductions were observed after 12 months of treatment (SMD - 0.56; CI -0.87, -0.24; MD -2.29 kg/m²). LT4 reduced BW in CH (SMD - 0.24; CI -0.34, -0.15; MD -2.15 kg), primarily in the first 3 months of treatment; it did not change FM and led to a small reduction in LM/FFM (SMD - 0.21; CI -0.37, -0.05). However, LT4 showed no significant effects on BMI, BW, FM, or LM/FFM in SCH, regardless of the analysis. Despite restoring thyroid hormonal homeostasis, LT4 showed limited efficacy in reversing the anthropometric alterations associated with CH and mainly SCH, suggesting that therapies beyond hormonal normalization may be required. Moreover, our data reinforces that LT4 monotherapy must not be prescribed for weight loss.</p>","PeriodicalId":21106,"journal":{"name":"Reviews in Endocrine & Metabolic Disorders","volume":" ","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149114229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}