Endocrinology and Metabolism

Original Article

Persistent Adipose Inflammation Despite Metabolic Recovery Reveals Tissue-Specific Immunomodulation by Tirzepatide: Mihye Seo, Maria Averia, Vivi Julietta, Shindy Soedono, Esther Jin Joo, Ellen Budiono, Minjoon Lee, Min-Kyu Kim, Yongsung Hwang, Hyeong Kyu Park, Kyoil Suh, Kae Won Cho; Received November 3, 2025 Accepted January 15, 2026 Published online May 15, 2026; DOI: https://doi.org/10.3803/EnM.2025.2766 [Epub ahead of print]

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Abstract PDF Supplementary Material PubReader ePub: Background
Obesity is characterized by chronic inflammation and fibrosis of adipose tissue; however, the extent to which these pathological features persist during pharmacologically induced weight loss remains poorly understood. This study investigated the effects of tirzepatide, a dual agonist of the glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide receptors, on adipose tissue inflammation and fibrosis in obese mice.
Methods
Diet-induced obesity was treated with tirzepatide or vehicle for 25 days. Metabolic parameters, tissue inflammation, fibrosis, and macrophage activation were assessed using histology, flow cytometry, gene expression analyses, and immunoblotting. In vitro experiments were conducted to compare the effects of tirzepatide on classically activated and metabolically activated macrophages.
Results
Tirzepatide significantly reduced body weight and adiposity, increased energy expenditure, and upregulated thermogenic and mitochondrial proteins in brown adipose tissue. Hyperglycemia and glucose intolerance were normalized. However, adipose tissue inflammation and fibrosis persisted despite weight loss, as evidenced by sustained immune cell infiltration, collagen deposition, and activation of Yes-associated protein (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) signaling. In contrast, hepatic inflammation and fibrosis were substantially improved. Mechanistically, tirzepatide suppressed inflammatory gene expression in classically activated macrophages but not in metabolically activated macrophages, suggesting that the local metabolic context determines tissue responsiveness to its anti-inflammatory actions.
Conclusion
Tirzepatide exerts distinct tissue-specific effects on inflammation and fibrosis during weight loss, ameliorating hepatic pathology while sparing adipose tissue inflammation. These findings identify metabolically activated macrophages as potential determinants of tissue-specific inflammatory persistence and underscore the need for therapeutic strategies that target macrophage activation and fibrotic remodeling to achieve durable metabolic benefits during pharmacological weight loss.

Review Article

Hypothalamus and pituitary gland
Growth Hormone, Not Simply Just a Hormone for Growth: Kevin C. J. Yuen, Jaime Guevara-Aguirre, John J. Kopchick; Endocrinol Metab. 2026;41(1):34-48. Published online February 3, 2026; DOI: https://doi.org/10.3803/EnM.2025.2806

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Abstract PDF PubReader ePub: Since its discovery almost 100 years ago, growth hormone (GH) has been extensively studied to elucidate its structural characteristics, receptor interactions and its physiologic and non-physiologic effects. These actions include but are not limited to its effects on somatic growth, substrate metabolism, body composition, bone mineral density, cardiovascular system, and cognitive function. Contextually, recombinant human GH was approved for growth promotion in children and to enhance metabolic health in adult patients with GH deficiency (GHD), along with other clinical indications. Studies involving individuals and animal models exhibiting dysregulated GH levels, ranging from complete or partial GHD to GH excess, have unveiled a spectrum of several less evident GH actions. In this review, we exclude discussing the classic GH therapeutic applications but instead focus on the interplay between GH and glucose metabolism, fibrosis, and carcinogenesis that is observed with varying GH levels and action. We also discuss clinical data derived from studies in acromegaly and GHD patients (including individuals with congenital GH and insulin-like growth factor I [IGF-I] deficiencies), and attempt to integrate findings from cellular, animal and human studies with the aim of highlighting novel characteristics and underlying molecular pathways through which both GH and IGF-I exert their more subtle actions.

Brief Report

Diabetes, obesity and metabolism
Characteristics of Metabolic Dysfunction-Associated Steatotic Liver Disease and Its Risk for Hepatic Fibrosis in 476,124 Korean Adults: A Cross-Sectional Study: Da Yeon Lee, Ji-Hee Ko, Han-Na Jang, Sun Joon Moon, Hye-Mi Kwon, Se Eun Park, Cheol-Young Park, Won-Young Lee, Ki-Won Oh, Eun-Jung Rhee; Endocrinol Metab. 2025;40(4):648-652. Published online March 27, 2025; DOI: https://doi.org/10.3803/EnM.2024.2281

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As the new terminology of metabolic dysfunction-associated steatotic liver disease (MASLD) and MASLD with increased alcohol intake (MetALD) has emerged, the clinical significance of MASLD is increasing. This cross-sectional study analyzed 476,124 health checkup participants (2002–2022) to compare hepatic fibrosis risks across MASLD, MetALD, non-alcoholic fatty liver disease (NAFLD), and metabolic dysfunction-associated fatty liver disease (MAFLD). Steatotic liver was identified via ultrasonography, and fibrosis risk was assessed using aspartate aminotransferase to platelet ratio index and NAFLD fibrosis score. The prevalence of NAFLD, MAFLD, MASLD, and MetALD was 30.1%, 32.3%, 29.8%, and 3.0%, respectively, with a 27.9% overlap among three conditions. Participants with steatotic liver were predominantly male, with higher glucose, lipids, liver enzymes, and homeostasis model assessment of insulin resistance levels. Three disease definitions largely overlapped, with MASLD and NAFLD being very similar, while participants with MAFLD and MetALD showed increased fibrosis risk (clinical trial registration number: 2024-11-050).

Citations

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Goh Eun Chung, Su Jong Yu, Jeayeon Park, Yoon Jun Kim, Jung‐Hwan Yoon, Kyungdo Han, Eun Ju Cho
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Original Articles

Diabetes, Obesity and Metabolism
The Impact of Insulin Resistance on Hepatic Fibrosis among United States Adults with Non-Alcoholic Fatty Liver Disease: NHANES 2017 to 2018: Ji Cheol Bae, Lauren A. Beste, Kristina M. Utzschneider; Endocrinol Metab. 2022;37(3):455-465. Published online June 21, 2022; DOI: https://doi.org/10.3803/EnM.2022.1434

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Background
We aimed to investigate the association of hepatic steatosis with liver fibrosis and to assess the interactive effects of hepatic steatosis and insulin resistance on liver fibrosis in a nationally representative sample of United States adults.
Methods
We conducted a cross-sectional analysis using data from National Health and Nutrition Examination Survey 2017 to 2018, which for the first time included transient elastography to assess liver stiffness and hepatic steatosis. We evaluated the association between hepatic steatosis (using controlled attenuation parameter [CAP]) and clinically significant liver fibrosis (defined as liver stiffness ≥7.5 kPa) using logistic regression with an interaction term for hepatic steatosis and insulin resistance (defined as homeostatic model assessment of insulin resistance ≥3.0).
Results
Among adults undergoing transient elastography (n=2,023), 45.9% had moderate or greater hepatic steatosis and 11.3% had clinically significant liver fibrosis. After adjustment for demographic and metabolic factors, the odds of significant liver fibrosis increased as CAP score rose (odds ratio, 1.35 per standard deviation increment; 95% confidence interval, 1.11 to 1.64). We detected a significant interaction effect between CAP score and insulin resistance on the probability of significant liver fibrosis (P=0.016 for interaction). The probability of significant liver fibrosis increased in the presence of insulin resistance with increasing CAP score, while those without insulin resistance had low probability of significant liver fibrosis, even with high CAP scores.
Conclusion
Individuals with hepatic steatosis had higher odds of fibrosis when insulin resistance was present. Our findings emphasize the importance of the metabolic aspects of the disease on fibrosis risk and suggest a need to better identify patients with metabolic associated fatty liver disease.

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Nicole Anna Dietzel, Maria Schmidt, Johannes Wiegand, Thomas Berg, Ronald Biemann, Ronny Baber, Michael Kluge, Kerstin Wirkner, Dirk Alexander Wittekind
Frontiers in Medicine.2026;[Epub] CrossRef
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Wei Yoon Poh, Shamsul Mohd Zain, Fatiha Hana Shabaruddin, Amirah Azzeri, Shir Ley Lee, Rosmawati Mohamed
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Yuou Ying, Yuan Ji, Ruyi Ju, Jinhan Chen, Mingxian Chen
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Haoxuan Zou, Jiejie Xie, Xiaopu Ma, Yan Xie, Xingshun Qi
Canadian Journal of Gastroenterology and Hepatology.2025;[Epub] CrossRef
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Diabetes, Obesity and Metabolism
Short-Chain Fatty Acids Attenuate Renal Fibrosis and Enhance Autophagy of Renal Tubular Cells in Diabetic Mice Through the HDAC2/ULK1 Axis: Xiaoying Ma, Qiong Wang; Endocrinol Metab. 2022;37(3):432-443. Published online May 16, 2022; DOI: https://doi.org/10.3803/EnM.2021.1336

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Background
This study investigated the effect of short-chain fatty acids (SCFAs) on diabetes in a mouse model.
Methods
Autophagy in Akita mice and streptozocin (STZ)-induced diabetic C57BL/6 mice was determined by Western blots and immunohistochemistry (IHC). Western blots, IHC, hematoxylin and eosin staining, Masson staining, periodic acid-Schiff staining, and picrosirius red staining were conducted to detect whether autophagy and renal function improved in Akita mice and STZ-induced diabetic C57BL/6 mice after treatment of SCFAs. Western blots, IHC, and chromatin immunoprecipitation were performed to determine whether SCFAs affected diabetic mice via the histone deacetylase (HDAC2)/unc-51 like autophagy activating kinase 1 (ULK1) axis. Diabetic mice with kidney-specific knockout of HDAC2 were constructed, and IHC, Masson staining, and Western blots were carried out to detect whether the deletion of endogenous HDAC2 contributed to the improvement of autophagy and renal fibrosis in diabetic mice.
Results
Reduced autophagy and severe fibrosis were observed in Akita mice and STZ-induced diabetic C57BL/6 mice. Increased autophagy and reduced renal cell fibrosis were found in SCFA-treated Akita diabetic mice and STZ-induced diabetic C57BL/6 mice. Diabetic mice treated with SCFAs had lower HDAC2 expression and more enriched binding of ULK1 promoter sequences to H3K27Ac. Endogenous knockout of HDAC2 caused enhanced autophagy and decreased renal fibrosis in diabetic mice treated with SCFAs.
Conclusion
SCFAs enhanced autophagy of renal tubular cells and attenuated renal fibrosis in diabetic mice through the HDAC2/ULK1 axis.

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Diabetes, Obesity and Metabolism
Changes in Insulin Resistance Index and the Risk of Liver Fibrosis in Patients with Nonalcoholic Fatty Liver Disease without Diabetes: Kangbuk Samsung Health Study: Dae-Jeong Koo, Mi Yeon Lee, Inha Jung, Sun Joon Moon, Hyemi Kwon, Se Eun Park, Eun-Jung Rhee, Won-Young Lee; Endocrinol Metab. 2021;36(5):1016-1028. Published online October 21, 2021; DOI: https://doi.org/10.3803/EnM.2021.1110

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Background
Fibrosis is the most important prognostic factor for nonalcoholic fatty liver disease (NAFLD). Insulin resistance plays a key role of fibrosis progression. We evaluated the association between changes in homeostasis model assessment of insulin resistance (HOMA-IR) values and changes in fibrosis status in NAFLD.
Methods
We analyzed the data of 15,728 participants with NAFLD (86% men, mean age 40.5 years) who had no diabetes at baseline and visited our centers for health check-ups both in 2012 and 2016. The participants were classified into four groups according to the degree of change in HOMA-IR values from baseline to the end of follow-up: G1 (<0), G2 (0–0.50), G3 (0.51–1.00), and G4 (>1.00). NAFLD was assessed by ultrasonography, and fibrosis status was evaluated by the NAFLD fibrosis score (NFS) and the aspartate aminotransferase to platelet ratio index (APRI).
Results
After the 4-year follow-up, the multivariable-adjusted odds ratio (OR) for progression of fibrosis probability increased with increasing HOMA-IR values (OR, 2.25; 95% confidence interval [CI], 1.87 to 2.71 for NFS; and OR, 2.55; 95% CI, 2.05 to 3.18 for APRI, G4). This tendency remained consistent throughout the subgroup analyses, except in those for female sex and a body mass index <25 kg/m². The OR for regression of fibrosis probability decreased with increasing HOMA-IR values (OR, 0.33; 95% CI, 0.25 to 0.43 for NFS, G4).
Conclusion
Changes in HOMA-IR values were associated with changes in fibrosis status in patients with NAFLD without diabetes, which underscores the role of insulin resistance in liver fibrosis.

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Endocrine Research
Suppression of Fibrotic Reactions of Chitosan-Alginate Microcapsules Containing Porcine Islets by Dexamethasone Surface Coating: Min Jung Kim, Heon-Seok Park, Ji-Won Kim, Eun-Young Lee, Marie Rhee, Young-Hye You, Gilson Khang, Chung-Gyu Park, Kun-Ho Yoon; Endocrinol Metab. 2021;36(1):146-156. Published online February 24, 2021; DOI: https://doi.org/10.3803/EnM.2021.879

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Background
The microencapsulation is an ideal solution to overcome immune rejection without immunosuppressive treatment. Poor biocompatibility and small molecular antigens secreted from encapsulated islets induce fibrosis infiltration. Therefore, the aims of this study were to improve the biocompatibility of microcapsules by dexamethasone coating and to verify its effect after xenogeneic transplantation in a streptozotocin-induced diabetes mice.
Methods
Dexamethasone 21-phosphate (Dexa) was dissolved in 1% chitosan and was cross-linked with the alginate microcapsule surface. Insulin secretion and viability assays were performed 14 days after microencapsulation. Dexa-containing chitosan-coated alginate (Dexa-chitosan) or alginate microencapsulated porcine islets were transplanted into diabetic mice. The fibrosis infiltration score was calculated from the harvested microcapsules. The harvested microcapsules were stained with trichrome and for insulin and macrophages.
Results
No significant differences in glucose-stimulated insulin secretion and islet viability were noted among naked, alginate, and Dexa-chitosan microencapsulated islets. After transplantation of microencapsulated porcine islets, nonfasting blood glucose were normalized in both the Dexa-chitosan and alginate groups until 231 days. The average glucose after transplantation were lower in the Dexa-chitosan group than the alginate group. Pericapsular fibrosis and inflammatory cell infiltration of microcapsules were significantly reduced in Dexa-chitosan compared with alginate microcapsules. Dithizone and insulin were positive in Dexa-chitosan capsules. Although fibrosis and macrophage infiltration was noted on the surface, some alginate microcapsules were stained with insulin.
Conclusion
Dexa coating on microcapsules significantly suppressed the fibrotic reaction on the capsule surface after transplantation of xenogenic islets containing microcapsules without any harmful effects on the function and survival of the islets.

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Clinical Study
Development of a Non-Invasive Liver Fibrosis Score Based on Transient Elastography for Risk Stratification in Patients with Type 2 Diabetes: Chi-Ho Lee, Wai-Kay Seto, Kelly Ieong, David T.W. Lui, Carol H.Y. Fong, Helen Y. Wan, Wing-Sun Chow, Yu-Cho Woo, Man-Fung Yuen, Karen S.L. Lam; Endocrinol Metab. 2021;36(1):134-145. Published online February 24, 2021; DOI: https://doi.org/10.3803/EnM.2020.887

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Background
In non-alcoholic fatty liver disease (NAFLD), transient elastography (TE) is an accurate non-invasive method to identify patients at risk of advanced fibrosis (AF). We developed a diabetes-specific, non-invasive liver fibrosis score based on TE to facilitate AF risk stratification, especially for use in diabetes clinics where TE is not readily available.
Methods
Seven hundred sixty-six adults with type 2 diabetes and NAFLD were recruited and randomly divided into a training set (n=534) for the development of diabetes fibrosis score (DFS), and a testing set (n=232) for internal validation. DFS identified patients with AF on TE, defined as liver stiffness (LS) ≥9.6 kPa, based on a clinical model comprising significant determinants of LS with the lowest Akaike information criteria. The performance of DFS was compared with conventional liver fibrosis scores (NFS, FIB-4, and APRI), using area under the receiver operating characteristic curve (AUROC), sensitivity, specificity, positive and negative predictive values (NPV).
Results
DFS comprised body mass index, platelet, aspartate aminotransferase, high-density lipoprotein cholesterol, and albuminuria, five routine measurements in standard diabetes care. Derived low and high DFS cut-offs were 0.1 and 0.3, with 90% sensitivity and 90% specificity, respectively. Both cut-offs provided better NPVs of >90% than conventional fibrosis scores. The AUROC of DFS for AF on TE was also higher (P<0.01) than the conventional fibrosis scores, being 0.85 and 0.81 in the training and testing sets, respectively.
Conclusion
Compared to conventional fibrosis scores, DFS, with a high NPV, more accurately identified diabetes patients at-risk of AF, who need further evaluation by hepatologists.

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Review Article

Diabetes, Obesity and Metabolism
Noninvasive Evaluation of Nonalcoholic Fatty Liver Disease: Dae Ho Lee; Endocrinol Metab. 2020;35(2):243-259. Published online June 24, 2020; DOI: https://doi.org/10.3803/EnM.2020.35.2.243

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Nonalcoholic fatty liver disease (NAFLD) is the most prevalent liver diseases and can progress to advanced fibrosis and end-stage liver disease. Thus, intensive research has been performed to develop noninvasive methods for the diagnosis of nonalcoholic steatohepatitis (NASH) and fibrosis. Currently, no single noninvasive tool covers all of the stages of pathologies and conditions of NAFLD, and the cost and feasibility of known techniques are also important issues. Blood biomarkers for NAFLD may be useful to select subjects who need ultrasonography (US) screening for NAFLD, and noninvasive tools for assessing fibrosis may be helpful to exclude the probability of significant fibrosis and to predict advanced fibrosis, thus guiding the decision of whether to perform liver biopsy in patients with NAFLD. Among various methods, magnetic resonance-based methods have been shown to perform better than other methods in assessing steatosis as well as in detecting hepatic fibrosis. Many genetic markers are associated with the development and progression of NAFLD. Further well-designed studies are needed to determine which biomarker panels, imaging studies, genetic marker panels, or combinations thereof perform well for diagnosing NAFLD, differentiating NASH and fibrosis, and following-up NAFLD, respectively.

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Original Article

Lobeglitazone, a Novel Peroxisome Proliferator-Activated Receptor γ Agonist, Attenuates Renal Fibrosis Caused by Unilateral Ureteral Obstruction in Mice: Kwi-Hyun Bae, Jung Beom Seo, Yun-A Jung, Hye-Young Seo, Sun Hee Kang, Hui-Jeon Jeon, Jae Man Lee, Sungwoo Lee, Jung-Guk Kim, In-Kyu Lee, Gwon-Soo Jung, Keun-Gyu Park; Endocrinol Metab. 2017;32(1):115-123. Published online February 28, 2017; DOI: https://doi.org/10.3803/EnM.2017.32.1.115

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Background

Renal tubulointerstitial fibrosis is a common feature of the final stage of nearly all cause types of chronic kidney disease. Although classic peroxisome proliferator-activated receptor γ (PPARγ) agonists have a protective effect on diabetic nephropathy, much less is known about their direct effects in renal fibrosis. This study aimed to investigate possible beneficial effects of lobeglitazone, a novel PPARγ agonist, on renal fibrosis in mice.

Methods

We examined the effects of lobeglitazone on renal tubulointerstitial fibrosis in unilateral ureteral obstruction (UUO) induced renal fibrosis mice. We further defined the role of lobeglitazone on transforming growth factor (TGF)-signaling pathways in renal tubulointerstitial fibrosis through in vivo and in vitro study.

Results

Through hematoxylin/eosin and sirius red staining, we observed that lobeglitazone effectively attenuates UUO-induced renal atrophy and fibrosis. Immunohistochemical analysis in conjunction with quantitative reverse transcription polymerase chain reaction and Western blot analysis revealed that lobeglitazone treatment inhibited UUO-induced upregulation of renal Smad-3 phosphorylation, α-smooth muscle actin, plasminogen activator inhibitor 1, and type 1 collagen. In vitro experiments with rat mesangial cells and NRK-49F renal fibroblast cells suggested that the effects of lobeglitazone on UUO-induced renal fibrosis are mediated by inhibition of the TGF-β/Smad signaling pathway.

Conclusion

The present study demonstrates that lobeglitazone has a protective effect on UUO-induced renal fibrosis, suggesting that its clinical applications could extend to the treatment of non-diabetic origin renal disease.

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Case Report

A Case of Idiopathic Myelofibrosis Associated with Acromegaly Patient.: Jun Young Song, Pyoung Rak Choi, Hong Jun You, Seong Hoon Shin, Yu Ri Kim, Young Sik Choi, Yo Han Park, Mi Hyang Kim, Bong Kwon Chun, Young Duk Joh; J Korean Endocr Soc. 2006;21(4):328-332. Published online August 1, 2006; DOI: https://doi.org/10.3803/jkes.2006.21.4.328

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Abstract PDF: Acromegaly is a chronic condition resulting from the excessive secretion of growth hormone and insulin like growth factor 1, generally from pituitary adenoma. Although there have been several reports suggesting the possible association of hematologic malignancies with acromegaly, myelofibrosis with acromegaly is very rare. Here we report 54-year-old male patient with myelofibrosis accompanied with acromegaly. We treated this patient with low dose thalidomide (50 mg/day) and prednisone (30 mg/day). We reported this case with literature review.

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