High protein diets have become popular for body weight maintenance and weight loss despite controversies regarding efficacy and safety. Although both weight gain and weight loss are determined by energy consumption and expenditure, data from rodent trials consistently demonstrate that the protein:carbohydrate ratio in high fat diets strongly influences body and fat mass gain per calorie eaten. Here, we review data from rodent trials examining how high protein diets may modulate energy metabolism and the mechanisms by which energy may be dissipated. We discuss the possible role of activating brown and so-called beige/BRITE adipocytes including non-canonical UCP1-independent thermogenesis and futile cycles, where two opposing metabolic pathways are operating simultaneously. We further review data on how the gut microbiota may affect energy expenditure. Results from human and rodent trials demonstrate that human trials are less consistent than rodent trials, where casein is used almost exclusively as the protein source. The lack of consistency in results from human trials may relate to the specific design of human trials, the possible distinct impact of different protein sources, and/or the differences in the efficiency of high protein diets to attenuate obesity development in lean subjects vs. promoting weight loss in obese subjects.
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http://dx.doi.org/10.3389/fphys.2018.01792 | DOI Listing |
Mol Cancer
January 2025
Department of Hematology, Qilu Hospital of Shandong University, No.117, West of Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Background: Drug resistance and immune escape continue to contribute to poor prognosis in AML. Increasing evidence suggests that exosomes play a crucial role in AML immune microenvironment.
Methods: Sanger sequencing, RNase R and fluorescence in situ hybridization were performed to confirm the existence of circ_0006896.
J Immunother Cancer
January 2025
Department of Pathology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, USA
Background: Concurrent (STK11, KL) mutant non-small cell lung cancers (NSCLC) do not respond well to current immune checkpoint blockade therapies, however targeting major histocompatibility complex class I-related chain A or B (MICA/B), could pose an alternative therapeutic strategy through activation of natural killer (NK) cells.
Methods: Expression of NK cell activating ligands in NSCLC cell line and patient data were analyzed. Cell surface expression of MICA/B in NSCLC cell lines was determined through flow cytometry while ligand shedding in both patient blood and cell lines was determined through ELISA.
Electromagn Biol Med
January 2025
Programa de Pós- Graduação em Biociências e Saúde, UNIOESTE, Cascavel, Brazil.
Objective: The aim of this study was to systematically review the preclinical studies that have applied the static magnetic field to wound healing.
Methods: The search strategy was performed in databases: PubMed, Embase, Scopus, Web of Science, LILACS, CINAHL and Cochrane Database, and in gray literature. The inclusion criteria were: Pre-clinical studies, either with a separate control/sham parallel-group or cross-over design in rodents that used magnets to treat skin injuries anywhere on the body.
Cancer Med
January 2025
Department of Gastroenterology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, People's Republic of China.
Background: The toxicity and drug resistance associated with oxaliplatin (L-OHP) limit its long-term use for colorectal cancer (CRC) patients. p53 mutation is a common genetic trait of CRC. PRIMA-1 (APR-246, eprenetapopt) restores the DNA-binding capacity of different mutant P53 proteins.
View Article and Find Full Text PDFChem Biol Drug Des
January 2025
Department of Anesthesiology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China.
Cerebral ischemia/reperfusion injury (IRI) is pathologically associated with ferroptosis. Dexmedetomidine (Dex) exerts neuroprotective activity after cerebral IRI. Our work focused on probing the pharmacologic effect of Dex on ferroptosis during cerebral IRI and the mechanisms involved.
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