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Non-canonical hepatic androgen receptor mediates glucagon sensitivity in female mice through the PGC1α/ERRα/mitochondria axis.
Cell Rep
January 2025
Westlake Laboratory of Life Sciences and Biomedicine, Hangzhou, Zhejiang, China; Key Laboratory of Growth Regulation and Translational Research of Zhejiang Province, School of Life Sciences, Westlake University, Hangzhou, Zhejiang, China; Institute of Basic Medical Sciences, Westlake Institute for Advanced Study, Hangzhou, Zhejiang, China; Research Center for Industries of the Future, Westlake University, Hangzhou, Zhejiang, China. Electronic address:
Glucagon has recently been found to modulate liver fat content, in addition to its role in regulating gluconeogenesis. However, the precise mechanisms by which glucagon signaling synchronizes glucose and lipid metabolism in the liver remain poorly understood. By employing chemical and genetic approaches, we demonstrate that inhibiting the androgen receptor (AR) impairs the ability of glucagon to stimulate gluconeogenesis and lipid catabolism in primary hepatocytes and female mice.
View Article and Find Full Text PDFAssociations of CAIDE dementia risk score with glucose and lipid‐related metabolic blood biomarkers in the FINGER study participants.
Alzheimers Dement
December 2024
Division of clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet and Stockholm University, Stockholm, Sweden
Background: The Cardiovascular risk factors, aging, and dementia (CAIDE) risk score is a validated tool estimating dementia risk. We investigated the association of CAIDE score with 12 markers of glucose and lipid metabolism, in the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) participants.
Methods: The FINGER trial had 1260 participants, aged 60–77 years, with a CAIDE score ≥6, without substantial cognitive impairment.
Investigating the effects of semaglutide in early Alzheimer’s disease using single‐cell transcriptomics and proteomics – rationale and design.
Alzheimers Dement
December 2024
Novo Nordisk A/S, Søborg, Denmark
Background: Evidence suggests glucagon‐like peptide 1 receptor agonists (GLP‐1RAs) may have therapeutic potential in Alzheimer’s disease (AD). Cumulative evidence has indicated a potential reduction in cognitive decline in people with AD, while real‐world evidence has shown decreased dementia risk in patients with type 2 diabetes. Non‐clinical data reveal that GLP‐1RAs impact neuroinflammation and other biological processes believed to be involved in AD pathophysiology, including effects on central and peripheral immune cells.
View Article and Find Full Text PDFClinical implications of mineralocorticoid receptor overactivation.
Clin Kidney J
January 2025
Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA.
The mineralocorticoid receptor (MR) is a nuclear transcription factor that plays a critical role in regulating fluid, electrolytes, blood pressure, and hemodynamic stability. In conditions such as chronic kidney disease (CKD) and heart failure (HF), MR overactivation leads to increased salt and water retention, inflammatory and fibrotic gene expression, and organ injury. The MR is essential for transcriptional regulation and is implicated in metabolic, proinflammatory, and pro-fibrotic pathways.
View Article and Find Full Text PDFThe protective effects of liraglutide in reducing lipid droplets accumulation and myocardial fibrosis in diabetic cardiomyopathy.
Cell Mol Life Sci
January 2025
Institute of Medicine, Chung Shan Medical University, No. 110, Sec. 1, Jianguo N. Rd, Taichung City, 402, Taiwan.
Background: Diabetes is a primary contributor to diabetic cardiomyopathy (DbCM), which is marked by metabolic imbalances such as elevated blood glucose and lipid levels, leading to significant structural and functional alterations in the myocardium. Elevated free fatty acids (FFAs) and hyperglycemia play critical roles in DbCM development, with FFAs inducing insulin resistance in cardiomyocytes and promoting lipid accumulation, resulting in oxidative stress and fibrosis. Current research suggests that glucagon-like peptide-1 (GLP-1) receptor agonists may effectively mitigate DbCM, although an effective treatment for this condition remains elusive, and the precise mechanisms of this protective effect are not fully understood.
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