Although obese sarcopenia is a major public health problem with increasing prevalence worldwide, the factors that contribute to the development of obese sarcopenia are still obscure. In order to clarify this issue, a high-fat-diet-induced obese sarcopenia mouse model was utilized. After being fed with a high-fat diet for 24 weeks, decreased motor functions and muscle mass ratios were found in the C57BL/6 mice. In addition, the expression of calsarcin-2 was significantly increased in their skeletal muscle, which was determined by a microarray analysis. In order to clarify the role of calsarcin-2 in muscle, lentiviral vectors containing the calsarcin-2 gene or short hairpin RNA targeted to calsarcin-2 were used to manipulate calsarcin-2 expressions in L6 myoblasts. We found that an overexpression of calsarcin-2 facilitated L6 myoblast differentiation, whereas a calsarcin-2 knockdown delayed myoblast differentiation, as determined by the expression of myogenin. However, the calsarcin-2 knockdown showed no significant effects on myoblast proliferation. In addition, to clarify the relationship between serum calsarcin-2 and sarcopenia, the bilateral gastrocnemius muscle mass per body weight in mice and appendicular skeletal muscle mass index in humans were measured. Although calsarcin-2 facilitated myoblast differentiation, the serum calsarcin-2 concentration was negatively related to skeletal muscle mass index in mice and human subjects. Taken together, calsarcin-2 might facilitate myoblast differentiation and appear to play a compensatory role in sarcopenia.

Hepatic dysfunction is commonly observed in subjects with hyperthyroidism. Hepassocin is a hepatokine playing an important role in metabolic diseases and exhibiting a hepatic protective effect. Nevertheless, the relationship between hepassocin and hyperthyroidism was still unknown. In the present study, a total of 36 subjects with Graves’ disease were enrolled, and we found that the alanine aminotransferase (ALT) levels were significantly decreased in parallel with the decrement in serum hepassocin concentrations at 6 months after standard treatment for hyperthyroidism. In addition, HepG2 cell line was used to investigate the role of hepassocin in hyperthyroidism-induced hepatic dysfunction. Treatment of hepassocin recombinant protein in HepG2 cells dose-dependently decreased triiodothyronine (T3)-induced ALT and aspartate aminotransferase (AST) elevation. Moreover, hepassocin significantly increased the expression of phosphoenolpyruvate carboxykinase (PEPCK) in a dose-dependent manner. Deletion of hepassocin in HepG2 cells reversed the effects of T3 on PEPCK expressions. Furthermore, we found that T3 increased the expression of hepassocin through a hepatocyte nuclear factor 1α-dependent pathway. Taken together, these results indicated a compensatory increase in serum hepassocin might have a protective role in hyperthyroidism-induced hepatic dysfunction.

People with diabetes (PWD) exhibit a higher prevalence of Hepatitis C virus (HCV) infection, making them a crucial population for HCV screening and micro-elimination efforts. In light of the first published interdisciplinary consensus on managing/screening HCV in PWD, this study aims to evaluate the results and identify effective strategies for incorporating HCV screening and treatment into an existing diabetes care model managed by case managers. This multicenter prospective program, initiated by a diabetes society, involved eighteen centers in Taiwan. Each center developed strategies to enhance HCV screening and streamline linkage to HCV care for PWD. Data on screening, diagnosis, and direct-acting antiviral (DAA) treatment were collected. Hospitals were ranked by the average number of monthly DAA treatments, and the strategies of the top five centers were compared with others. Over a median period of 6.1 months, 28,436 patients were screened, and 1379 (4.8 %) tested positive for anti-HCV antibodies (Ab). A total of 333 (24.1 %) patients were positive for HCV RNA, of whom 288 (86.4 %) received DAA treatment. Overall, 25 strategies were adopted, with the more effective being: the involvement of multidisciplinary healthcare professionals in the program, automation of information technology to search for HCV history, and patient recall for HCV Ab screening. This program pioneered the evaluation of integrating of HCV screening and treatment in PWD, providing strategic insights into HCV micro-elimination through efficient patient identification and collaborative HCV management.

Background: Primary aldosteronism (PA) is a common cause of secondary hypertension and hypokalemia, but it rarely presents with neuromuscular symptoms. Although only a few cases of hypokalemia‐induced rhabdomyolysis have been reported, dropped head syndrome (DHS) due to cervical axial muscle weakness has not previously been described in the context of PA. Case Presentation: A 65‐year‐old woman with a history of hypertension presented with progressive posterior neck weakness, followed by proximal limb soreness and weakness. Cervical spine disease was initially suspected, but CT imaging revealed only degenerative changes without cord compression. Laboratory tests showed severe hypokalemia (1.5 mmol/L), metabolic alkalosis, and markedly elevated creatine kinase and myoglobin levels, consistent with rhabdomyolysis. Her symptoms resolved after potassium supplementation. Endocrine workup revealed an elevated aldosterone‐to‐renin ratio (ARR) and a positive captopril suppression test. CT and NP‐59 SPECT/CT identified a left adrenal functioning adenoma. Laparoscopic adrenalectomy confirmed an aldosterone‐producing adrenal cortical adenoma. Postoperatively, the patient achieved complete biochemical remission with normalized potassium levels, improved blood pressure, and no recurrence of muscle weakness or neck symptoms. Conclusion: This case highlights a rare presentation of PA as hypokalemia‐induced rhabdomyolysis and DHS mimicking cervical spine pathology. In patients with unexplained focal muscle weakness and persistent hypokalemia, particularly in the setting of hypertension, PA should be considered. Clinicians should maintain a high index of suspicion and pursue comprehensive diagnostic evaluations. Early diagnosis and definitive treatment can prevent long‐term complications and enable full metabolic recovery.

Background: Recently, the incidence of diabetes has increased. A rapid method for the diagnosis of prediabetes is needed. Although granulin levels are associated with obesity and insulin resistance, it remains unclear whether serum granulin concentration may serve as a biomarker of prediabetes and diabetes. Here, we examined the association between serum granulin and glycemic status in a clinical population. Methods: In total, 180 age- and sex-matched participants with normal glucose tolerance (NGT), impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and newly diagnosed diabetes (NDD) were recruited. Serum granulin levels were measured via an enzyme-linked immunosorbent assay. Multivariate linear regression analysis was performed to evaluate the relationships between the level of granulin and different glycemic statuses. The utility of the granulin concentration for diagnosis of prediabetes and diabetes was evaluated with a receiver operating characteristic (ROC) curve. Results: Serum granulin concentrations were significantly greater in the IFG, IGT and NDD groups than in the NGT group. Multiple linear regression analysis revealed that obesity and glycemic status were independently associated with granulin concentrations. The ROC curve analysis revealed an area under the curve of 0.781 (95% CI, 0.709–0.853; p < 0.001). Conclusions: An elevated serum granulin concentration has potential utility as a biomarker for screening prediabetes and diabetes.