Did the prebiotic diet (GOS/PDX) attenuate any adverse effects of 3g exposure on host physiology?

Label:chem

Topic
3g exposure caused weight loss, reduced food intake, and altered red blood cell parameters like MCH.
Answer
While the prebiotic diet did not prevent 3g-induced weight loss, it modestly attenuated the decrease in mean corpuscular hemoglobin (MCH) and maintained NLR at lower levels, suggesting partial protection against stress-induced physiological disruptions.
Return to Home Chemical List
Knowledge you may be interested in
What are galactooligosaccharides (GOS) and polydextrose (PDX)? How does biotin supplementation interfere with laboratory allergy diagnostics? Can excess or deficiency of biotin influence immune responses and allergy? Does biotin (or its precursors) act as an allergen or hapten? How does biotin interact with avidin and streptavidin? How stable is biotin under various physical conditions? What is the chemical structure and identity of biotin? Does Astragaloside IV (AS-IV) show sex-dependent effects on EEG? What are the acute neurophysiological effects of Astragaloside IV (AS-IV) on EEG? Can Astragaloside IV (AS-IV) cross the blood–brain barrier (BBB)? What is diallyl disulfide (DADS), and what are its antitumoral properties? How does diallyl disulfide (DADS) affect cell viability in colorectal cancer cell lines (Caco-2 and HT-29) and non-tumoral HUVEC cells? Does diallyl disulfide (DADS) induce DNA damage in colorectal cancer cell lines? How is fasting glucose estimated from hemoglobin A1c (HbA1c)? What is tirzepatide (TZP) chemically, and by which biochemical mechanism does it exert its hepatic effects? What is the quantitative effect of TZP + LEKT versus TZP + LCD on hepatic fat content as measured by the controlled attenuation parameter (CAP)? What is trans-sodium crocetinate (TSC) and how does it differ from trans-crocetin? What is the primary signaling pathway targeted by trans-sodium crocetinate (TSC) to alleviate high-altitude acute lung injury (HALI)? How was maternal dietary intake of fatty acids assessed, and which fatty acids were quantified? Which placental phospholipid fatty acids showed significant correlations with maternal dietary intake?