Tracing the activation mechanism of mitochondrial stress response and longevity in C. elegans. Credit: Terytty Yang Li and Arwen W. Gao, EPFL Scientists.
Study explains why antipsychotic medications lead to weight gain, promote metabolic syndrome
Why do patients who receive antipsychotic medications to manage schizophrenia and bipolar disorder quickly gain weight and develop prediabetes and hyperinsulemia? The question remained a mystery for decades, but in a paper published today in
Translational Psychiatry, researchers from the University of Pittsburgh School of Medicine finally cracked the enigma.
Antipsychotic drugs, scientists showed, not only block dopamine signaling in the brain but also in the pancreas, leading to uncontrolled production of blood glucose-regulating hormones and, eventually, obesity and diabetes.
There are dopamine theories of schizophrenia, drug addiction, depression and neurodegenerative disorders, and we are presenting a dopamine theory of metabolism. We re seeing now that it is not only interesting to study dopamine in the brain, but it is equally interesting and important to study it in the periphery.
Kruppel-like factor 15 controls skeletal muscle fat uptake and utilization
Metabolic diseases, such as obesity and type 2 diabetes, have risen to epidemic proportions in the U.S. and occur in about 30 percent of the population. Skeletal muscle plays a prominent role in controlling the body s glucose levels, which is important for the development of metabolic diseases like diabetes.
In a recent study, published in
The Journal of Clinical Investigation, University Hospitals (UH) Cleveland Medical Center and Case Western Reserve University School of Medicine researchers have found that skeletal muscle significantly affects how the body stores and metabolizes fat.
In the study, Mukesh K. Jain, MD, senior author, Chief Academic Officer at UH, and the Ellery Sedgwick Jr. Chair & Distinguished Scientist, and his team set out to investigate the role of a gene called Kruppel-like factor 15 (KLF15) in skeletal muscle. The team utilized a mouse model with KLF15 specifically deleted in musc