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Background: The interplay between obesity and thyroid dysfunction is complex, characterized by adaptive hyperthyrotropinemia and peripheral hormone resistance. Metabolic and Bariatric surgery (MBS) has emerged not only as a weight-loss (WL) intervention but also as a potent modulator of the thyroid–gut axis. Methods: We conducted a narrative review of the literature (2015–2025), synthesizing data from prospective cohorts, meta-analyses, and mechanistic studies to evaluate the impact of MBS on thyroid function, autoimmune dynamics, and drug pharmacokinetics. Discussion: Current evidence suggests that MBS promotes a recalibration of the thyroid axis. Post-operative WL is independently associated with a significant reduction in serum thyroid-stimulating hormone (TSH) and free triiodothyronine (fT3) levels, reversing obesity-induced peripheral resistance. Concurrently, the reduction in systemic inflammation (NOD-like receptor protein 3 (NLRP3) inflammasome deactivation) may dampen lymphocytic infiltration, while the amelioration of gut dysbiosis and intestinal permeability is hypothesized to reduce cross-reactivity mechanisms (molecular mimicry), leading to decreased antibody titers in Hashimoto’s thyroiditis. However, these benefits are counterbalanced by altered drug absorption mechanisms. While most hypothyroid patients benefit from reduced Levothyroxine (L-T4) requirements due to decreased lean mass, malabsorptive procedures (Roux-en-Y Gastric Bypass, One Anastomosis Gastric Bypass) can precipitate refractory hypothyroidism due to bypassed absorptive surfaces and altered gastric pH. Conclusions: MBS offers a dual benefit of functional restoration and modulation of autoimmune markers. However, post-surgical management requires a tailored approach. Clinicians must distinguish between the physiological decline in TSH (adaptive) and iatrogenic malabsorption, advocating for liquid L-T4 formulations in complex malabsorptive phenotypes.

6 February 2026

Pathophysiology of the Thyroid–Gut Axis in Obesity. The diagram illustrates the central and peripheral alterations involving the hypothalamus, pituitary, thyroid gland, and target tissues. Note the distinction between peripheral thyroid hormone resistance (reduced sensitivity to T3/T4 in liver and skeletal muscle, often associated with altered deiodinase activity and metabolic syndrome [22]) and the compensatory glandular hyperactivity of the thyroid in response to elevated TSH and leptin stimulation. The figure highlights how obesity-induced inflammation and dysbiosis contribute to resetting the central TSH set-point.
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Objectives: This study aimed to evaluate adherence to therapy in hypoparathyroidism and related endocrine–metabolic disorders and to assess its association with biochemical outcomes, hypocalcemia episodes, and health-related quality of life (HRQoL). Methods: In accordance with PRISMA 2020 guidelines, PubMed, Scopus, Google Scholar, and the Cochrane Library were searched until September 2025. The eligible studies were randomized controlled trials, cohort, case–control studies, cross-sectional, and observational studies that reported adherence to calcium/vitamin D or recombinant parathyroid hormone therapy. Results: twenty-three studies were included in the qualitative synthesis, and 11 studies were included in the quantitative meta-analysis. Pooled medication adherence compliance was 70–82% and improved with simplified regimens and the use of recombinant PTH. Additionally, this was also associated with an improvement in HRQoL (p < 0.0001) and a lower risk of hypocalcemia (p < 0.0001). Conversely, multifactorial regulation was observed as the level of adherence had no significant effect on serum calcium levels (p = 0.7116). Sensitivity analyses demonstrate the strength of findings and indicate no significant publication bias. Conclusions: Medication adherence is a key factor in determining patient-centered outcomes in hypoparathyroidism. Better adherence is linked to a higher quality of life and fewer episodes of hypocalcemia, while its effect on biochemical parameters seems minimal. Educational programs, simple treatment regimens, and wider access to rhPTH therapy can be used to improve patient management of the disease over time.

26 January 2026

Diabetic foot complications represent a major global health burden and arise from a multifactorial interaction between neuropathy, ischemia, infection, and impaired wound repair. Increasing evidence suggests that, beyond traditional vascular and metabolic risk factors, endocrine dysregulation plays a central role in shaping vascular dysfunction and tissue vulnerability in patients with diabetes. This narrative review provides an updated overview of the endocrine–vascular axis in the development, progression, and healing of diabetic foot ulcers (DFUs), integrating evidence from experimental and clinical studies identified through targeted searches of PubMed, Embase, and Scopus. We examine how alterations in insulin signaling, relative glucagon excess, adipokine imbalance, dysregulation of stress hormones, and thyroid dysfunction interact with chronic hyperglycemia, dyslipidemia, mitochondrial dysfunction, and low-grade inflammation to impair endothelial homeostasis. These disturbances promote oxidative stress, reduce nitric oxide bioavailability, and compromise microvascular perfusion, thereby creating a pro-ischemic and pro-inflammatory tissue environment that limits angiogenesis, extracellular matrix (ECM) remodeling, immune coordination, and effective wound repair. By linking pathophysiological mechanisms to clinical relevance, this review highlights potential biomarkers of endocrine–vascular dysfunction, implications for risk stratification, and emerging therapeutic perspectives targeting metabolic optimization, endothelial protection, and hormonal modulation. Finally, key knowledge gaps and priority areas for future translational and clinical research are discussed, supporting the development of integrated endocrine-based strategies aimed at improving DFU prevention, healing outcomes, and long-term limb preservation in patients with diabetes.

25 January 2026

Endocrines was launched five years ago with a clear goal: to offer an open, rigorous, and inclusive forum for research spanning basic, translational, and clinical endocrinology and metabolism [...]

19 January 2026

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Update on X-linked Hypophosphatemia
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Update on X-linked Hypophosphatemia

Editors: Yukihiro Hasegawa, Seiji Fukumoto

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Endocrines - ISSN 2673-396X