Adverse maternal nutrition induces developmental programming in progeny thereby predisposing them to metabolic disease. The aim of the study was to determine whether maternal diets, with varying fat percentages as energy, alter the expression of factors associated with brain glucose sensing (glucose transporter 2 and glucokinase) and the feeding response (neuropeptide Y and leptin). Pregnant dams were maintained on diets of 10% (control), 20% (20F), 30% (30F) and 40% (40F) fat as energy throughout gestation. In 1-day-old neonatal offspring, anthropometric measurements were recorded. Whole neonatal brain was rapidly excised, weighed and either snap-frozen at -80°C for quantitative RT-PCR or fixed in formalin for immunohistochemical analysis. Brain glucose transporter 2, glucokinase, neuropeptide Y and leptin mRNA expression and immunoreactivity were determined in neonates. In the 20F neonates increases in body weight, head circumference and crown to rump length concomitant with reduced glucokinase immunoreactivity were found. The 30F neonates displayed increases in body weight, head length, head width, crown to rump length and immunoreactivity for both glucose transporter 2 and neuropeptide Y. The 40F neonates also demonstrated increased glucose transporter 2 and neuropeptide Y immunoreactivity. Fetal exposure to a gestational diet with 30% or 40% fat as energy results in increased immunoreactivity for brain glucose transporter 2 and neuropeptide Y, suggesting a programming effect of these diets that may represent an early event of obesity.
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http://dx.doi.org/10.1016/j.ijdevneu.2010.07.226 | DOI Listing |
Curr Drug Metab
January 2025
Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran.
Quercetin (QE), a particular flavonoid, is well known for its medicinal effects, including anti-oxidant, hypoglycemic, and anti-inflammatory effects. In this review, the findings of QE effects on diabetes STZinduced, alloxan-induced, and its complications have been summarized with a particular focus on in vitro, in vivo, and clinical trials. Consequently, QE mediates several mechanisms, including ameliorating tumor necrosis factor (TNF)-α, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), interleukin (IL)-1β, IL-8, and IL-10 expression, increasing insulin glucose uptake to inhibit insulin resistance.
View Article and Find Full Text PDFBurns Trauma
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Department of Critical Care Medicine, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, No. 321 Zhongshan Road, Gulou District, Nanjing, Jiangsu 210008, China.
Background: Non-thyroidal illness syndrome is commonly observed in critically ill patients, characterized by the inactivation of systemic thyroid hormones (TH), which aggravates metabolic dysfunction. Recent evidence indicates that enhanced TH inactivation is mediated by the reactivation of type 3 deiodinase (Dio3) at the tissue level, culminating in a perturbed local metabolic equilibrium. This study assessed whether targeted inhibition of Dio3 can maintain tissue metabolic homeostasis under septic conditions and explored the mechanism behind Dio3 reactivation.
View Article and Find Full Text PDFInt J Nanomedicine
January 2025
Department of Biopharmacy, School of Pharmaceutical Sciences, Jilin University, Changchun, People's Republic of China.
Diabetol Int
January 2025
Department of Endocrinology and Diabetes, NTT Medical Center Tokyo, 141-86255-9-22 Higashi-Gotanda, Shinagawa-ku, Tokyo Japan.
A 73-year-old Japanese woman was admitted to our hospital with anorexia, weight loss, and fever. A few weeks prior to admission, she became aware of anorexia. She was leukopenic, complement-depleted, and positive for antinuclear antibodies and anti-double stranded DNA antibodies.
View Article and Find Full Text PDFDiabetol Int
January 2025
Department of Pediatrics, Hamamatsu University School of Medicine, 1-20-1 Handayama, Chuo-Ku, Hamamatsu, 431-3192 Japan.
We report a beneficial effect of a sodium glucose co-transporter 2 (SGLT2) inhibitor in the management of insulin resistant diabetes mellitus (IRDM) in a Japanese girl with mild Rabson-Mendenhall syndrome (RMS). At 10 2/12 years of age, she was referred to us because of glucosuria, and was found to have marked acanthosis nigricans and RMS-like facial features such as proptosis, large ears, full lips, and gingival hypertrophy, but not other clinical features frequently found in RMS. At 11 9/12 years of age, her blood HbA1c level, though it remained ~ 6.
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