The hypoglycemic mechanism of catalpol involves increased AMPK-mediated mitochondrial biogenesis.

Mitochondria serve as sensors of energy regulation and glucose levels, which are impaired by diabetes progression. Catalpol is an iridoid glycoside that exerts a hypoglycemic effect by improving mitochondrial function, but the underlying mechanism has not been fully elucidated. In the current study we explored the effects of catalpol on mitochondrial function in db/db mice and C2C12 myotubes in vitro. After oral administration of catalpol (200 mg·kg-1·d-1) for 8 weeks, db/db mice exhibited a decreased fasting blood glucose level and restored mitochondrial function in skeletal muscle. Catalpol increased mitochondrial biogenesis, evidenced by significant elevations in the number of mitochondria, mitochondrial DNA levels, and the expression of three genes associated with mitochondrial biogenesis: peroxisome proliferator-activated receptor gammaco-activator 1 (PGC-1α), mitochondrial transcription factor A (TFAM) and nuclear respiratory factor 1 (NRF1). In C2C12 myotubes, catalpol significantly increased glucose uptake and ATP production. These effects depended on activation of AMP-activated protein kinase (AMPK)-mediated mitochondrial biogenesis. Thus, catalpol improves skeletal muscle mitochondrial function by activating AMPK-mediated mitochondrial biogenesis. These findings may guide the development of a new therapeutic approach for type 2 diabetes.

Endobronchial hamartoma mimicking malignant lung tumor contralateral endobronchial metastasis: A case report.

RATIONALE: Endobronchial hamartoma, the most common benign lung tumor, is located in the bronchus, and it easily mimics lung cancer or bronchial metastasis. Endobronchial hamartoma can cause coughing, hemoptysis, and pulmonary infection; thus, it should be treated right away by surgery or fiberoptic bronchoscopy. PATIENT CONCERNS: We report a rare case of endobronchial hamartoma in which the clinical symptoms and imaging overlapped strongly with malignant lung tumor contralateral endobronchial metastasis. DIAGNOSES: Endobronchial hamartoma coexisting with a malignant lung tumor. INTERVENTIONS: Fiberoptic bronchoscopy was conducted, and the pathologic diagnosis was hamartoma. A second fiberoptic bronchoscopy was conducted, and fine-needle aspiration cytology of the enlarged lymph nodes indicated squamous cell carcinoma. OUTCOMES: The clinical symptoms were relieved, and the treatment options were docetaxel, cis-dichlorodiamineplatinum, and endostatin. LESSONS: Fiberoptic bronchoscopy needs to be guided by imaging and can be considered an effective method for the diagnosis of endobronchial hamartoma.