Sterol regulatory element binding protein-1c (SREBP-1c) is a transcription factor that responds to nutritional status and regulates metabolic gene expression in liver and adipose tissue. Although SREBP-1c RNA is expressed in skeletal muscle, little is known about its regulation in this tissue. To determine whether SREBP-1c is regulated by nutritional status in muscle, rats were food deprived for 48 h and then given access to a semipurified high cornstarch diet for 0, 6, 12 or 24 h. At each time point, blood was drawn for measurement of glucose and insulin concentrations, and the soleus, gastrocnemius and the white portion of the quadriceps muscle were removed for measurement of SREBP-1c RNA and protein. SREBP-1c RNA was increased (P < 0.05) by 6 h of refeeding and peaked at 12 h (fivefold in soleus and gastrocnemius, fourfold in white vastus) in all muscles studied. SREBP-1a RNA was not altered by refeeding. In accordance with the RNA data, the 125-kDa SREBP-1 protein increased with refeeding. To determine whether food deprivation decreased SREBP-1c RNA, rats were fed a high cornstarch diet during their normal diurnal cycle. Food was withdrawn at the beginning of the light cycle and muscles collected at 0, 6, 12 and 24 h after food was removed. SREBP-1c RNA decreased at all time points and was approximately 60% lower in the soleus and gastrocnemius and approximately 75% lower in the white quadriceps after 24 h. Additional refeeding experiments were conducted using a high fat diet in place of a high cornstarch diet. This diet diminished the increase in SREBP-1c RNA at all time points and in all muscles. This effect could not be explained by plasma glucose or insulin concentration. In conclusion, SREBP-1c RNA and SREBP-1 protein levels respond to nutritional status in skeletal muscle.
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http://dx.doi.org/10.1093/jn/133.6.1787 | DOI Listing |
Cell Mol Biol Lett
December 2024
Department of Hematology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Add: No.324, Jingwu Road, Jinan, 250021, Shandong, China.
Background: Disorders of lipid metabolism are critical factors in the progression of chronic lymphocytic leukemia (CLL). However, the characteristics of lipid metabolism and related regulatory mechanisms of CLL remain unclear.
Methods: Hence, we identified altered metabolites and aberrant lipid metabolism pathways in patients with CLL by ultra-high-performance liquid chromatography-mass spectrometry-based non-targeted lipidomics.
J Ethnopharmacol
December 2024
State Key Laboratory of Traditional Chinese Medicine Syndrome, The First Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, China; Department of Endocrinology, First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China; ShenShan Hospital, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Shanwei, 516600, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, 510405, China. Electronic address:
Phytomedicine
November 2024
Department of Molecular Biology and Cell Research, Chang Bing Show-Chwan Memorial Hospital, Changhua, Taiwan; Department of Hematology‑Oncology, Chang Bing Show Chwan Memorial Hospital, Changhua, Taiwan.
Background: Oral cancer is a malignant tumor of the oral cavity, with regulatory T cell (Treg) infiltration associated with poor prognosis. Ginkgolide B (GB) has demonstrated effects on lipid metabolism; however, its potential immunotherapeutic effects on oral cancer have not been elaborated.
Purpose: This study aimed to explore the immunotherapeutic effects of Ginkgolide B (GB) in oral cancer.
Lipids Health Dis
November 2024
Department of Endocrinology, The Third Xiangya Hospital of Central South University, No. 138 Tongzipo Road, Yuelu District, Changsha, Hunan, 410013, People's Republic of China.
Background: Metabolic dysfunction associated steatotic liver disease (MASLD), closely linked to excessive lipogenesis, induces chronic liver disease. MASLD often cause other metabolic diseases, such as cardiovascular disease, diabetes and obesity. However, the mechanism of N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) mRNA modification in lipogenesis of MASLD has not been fully elucidated.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
October 2024
Central Laboratory, First College of Clinical Medical Science of China Three Gorges University (Yichang Central People's Hospital)//Hubei Key Laboratory of Ischemic Cardiovascular Disease//Hubei Provincial Clinical Research Center for Ischemic Cardiovascular Disease, Yichang 443003, China.
Objective: To investigate the mechanism of Nlrp6 for regulating hepatocellular carcinoma (HCC) progression in light of lipid synthesis regulation.
Methods: Nlrp6 expression level in HCC tissues of different pathological grades was investigated using RNA-seq data from The Cancer Genome Atlas (TCGA) database, and its correlation with the patients' survival was analyzed with Kaplan-Meier survival analysis. HepG2 cells with adenovirus-mediated Nlrp6 overexpression or knockdown were treated with palmitic acid (PA), and the changes in lipid deposition and cell proliferation were evaluated using Oil Red O staining, CCK-8 assay, EdU staining, and colony formation assay.
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