Objective: Growth hormone secretion is decreased in obese subjects, and their GH response to stimulation tests is blunted. The mechanisms relating excess adipose mass and GH secretion are unknown. We hypothesized that leptin might be a signal linking adipose mass to GH secretion.
Design: We measured serum leptin levels and the GH response to stimulation tests in 42 obese and 40 lean short normal prepubertal children.
Results: The mean serum leptin concentrations were 23.8+/-1.7 ng/ml and 3.6+/-0.4 ng/ml in obese and lean children respectively, and were found to be inversely related to GH peak in both groups. After adjusting for body fat data, leptin was still an independent predictor of GH peak. Multiple stepwise regression analysis identified both leptin (regression coefficient = -0.78, P = 0.001), and insulin (regression coefficient = -0.03. P = 0.009) as negative determinants of GH response to the GHRH test in obese children (multiple R = 0.64), and only leptin in lean children (r = -0.51, P = 0.001). No correlation was observed between leptin and IGF-I or IGF binding protein-3.
Conclusion: These results are consistent with the hypothesis that leptin could contribute to the regulation of GH secretion.
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http://dx.doi.org/10.1530/eje.0.1390591 | DOI Listing |
Cell Rep
January 2025
Department of Oncology, Cross Cancer Institute, University of Alberta, Edmonton, AB T6G 1Z2, Canada; Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, AB T6G 2R3, Canada. Electronic address:
Patients with colorectal cancers (CRCs) that have microsatellite instability (MSI) (MSI CRCs) face a better prognosis than those with the more common chromosomal instability (CIN) subtype (CIN CRCs) due to improved T cell-mediated anti-tumor immune responses. Previous investigations identified the cytosolic DNA (cyDNA) sensor STING as necessary for chemokine-mediated T cell recruitment in MSI CRCs. Here, we find that cyDNA from MSI CRC cells is inherently more capable of inducing STING activation and improves cytotoxic T cell activation by dendritic cells (DCs).
View Article and Find Full Text PDFCancer Biol Ther
December 2025
Department of Pharmacology, Physiology, and Cancer Biology, Thomas Jefferson University, Philadelphia, PA, USA.
Adaptive immune resistance in cancer describes the various mechanisms by which tumors adapt to evade anti-tumor immune responses. IFN-γ induction of programmed death-ligand 1 (PD-L1) was the first defined and validated adaptive immune resistance mechanism. The endoplasmic reticulum (ER) is central to adaptive immune resistance as immune modulatory secreted and integral membrane proteins are dependent on ER.
View Article and Find Full Text PDFPituitary
January 2025
Departments of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland.
Background: Arginine infusion stimulates copeptin secretion, a surrogate marker of arginine vasopressin (AVP), thereby serving as a diagnostic test in the differential diagnosis of suspected AVP deficiency (AVP-D). Yet, the precise mechanism underlying the stimulatory effect of arginine on the vasopressinergic system remains elusive. Arginine plays a significant role in the urea cycle and increases the production of urea.
View Article and Find Full Text PDFNat Commun
January 2025
Type 2 Immunity Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA.
How macrophages in the tissue environment integrate multiple stimuli depends on the genetic background of the host, but this is still poorly understood. We investigate IL-4 activation of male C57BL/6 and BALB/c strain specific in vivo tissue-resident macrophages (TRMs) from the peritoneal cavity. C57BL/6 TRMs are more transcriptionally responsive to IL-4 stimulation, with induced genes associated with more super enhancers, induced enhancers, and topologically associating domains (TAD) boundaries.
View Article and Find Full Text PDFJ Prev Alzheimers Dis
February 2025
Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX, USA; School of Behavioral and Brain Sciences, University of Texas at Dallas, Dallas, TX, USA.
Background: Recent disease-modifying treatments for Alzheimer's disease show promise to slow cognitive decline, but show no efficacy towards reducing symptoms already manifested.
Objectives: To investigate the efficacy of a novel noninvasive brain stimulation technique in modulating cognitive functioning in Alzheimer's dementia (AD).
Design: Pilot, randomized, double-blind, parallel, sham-controlled study SETTING: Clinical research site at UT Southwestern Medical Center PARTICIPANTS: Twenty-five participants with clinical diagnoses of AD were enrolled from cognition specialty clinics.
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