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Mehboob, S.

Publications and source records attributed to Mehboob, S..

3 recordsLinked to original sources

Fructooligosaccharide Supplementation Improves Glucose Homeostasis in Human-Relevant hyperglycemic Diet-Induced Obese Mice

Fructooligosaccharides (FOS) are prebiotic fibers that influence gut microbiota and host metabolic function. In a diet-induced obesity (DIO) mouse study, FOS supplementation was compared with PBS-treated obese controls. Blood glucose was markedly lower at Day 42 (221.9 {+/-} 7.8 vs 138.3 {+/-} 9.0 mg/dL), and remained lower at Day 56. FOS reduced body-weight gain from 8.4 {+/-} 0.9 g in PBS controls to 2.6 {+/-} 0.2 g, corresponding to an approximate 69.5% reduction in gain over Days 1-70. Cumulative feed consumption was not significantly different between PBS and FOS cages, suggesting that the observed metabolic effects were not explained simply by reduced food intake. These data support our thesis that FOS works as an active metabolic ingredient acting through the gut-liver-metabolic axis. Thus, in the present study, dietary FOS supplementation produced marked improvements in glucose homeostasis in a severe DIO model characterized by diabetic-range hyperglycemia that more closely resembles poorly controlled human type 2 diabetes. HIGHLIGHTSO_LIFructooligosaccharide (FOS) normalized glucose levels in a severe DIO model that mimics poorly controlled human type 2 diabetes. C_LIO_LIDay-42 blood glucose was reduced by [~]37.7% in FOS-treated DIO mice. C_LIO_LIFOS reduced body-weight gain by [~]69.5% versus controls over 70 days. C_LIO_LIMetabolic benefits occurred without a statistically significant reduction in feed intake. C_LIO_LIFindings support a gut-liver-metabolic mechanism rather than simple caloric restriction. C_LIO_LIData position FOS as an active metabolic ingredient with potential utility in diabetes and metabolic health. C_LI

pharmacology and toxicology↗

UT-018 Protects Collagen Extracellular Matrix Through Substrate-Directed Stabilization and Collagenase Modulation

Pathological collagen degradation is a central feature of impaired wound healing, dermal aging, periodontal breakdown, intestinal barrier injury and connective tissue degeneration. Current strategies often focus on direct inhibition of matrix metalloproteinases or collagenases; however, complete blockade of collagen remodeling may interfere with normal repair. UT-018, a bioactive formulation that acts as a tissue-protective and regenerative agent, was evaluated as a collagenous extracellular matrix modulator. Across in vitro kinetic assays, endpoint signal analysis, integrated area-under-curve (AUC) analysis and substrate preincubation studies, UT-018 produced concentration-dependent preservation of collagen against collagenase challenge. Importantly, collagen protection persisted after substrate preincubation with UT-018, with approximately 33%, 60% and 65% protection at 5, 10 and 25 mM UT-018 concentrations, respectively. Exploratory kinetic transformations did not support a simple competitive collagenase inhibitor model. Instead, the collective pattern supports a substrate-directed mechanism involving collagen shielding, reduced cleavage susceptibility and indirect modulation of collagenase activity. These findings position UT-018 as a potential first-in-class collagen resilience modulator for wound healing, gastrointestinal barrier protection, oral care, dermal preservation and regenerative medicine applications. Highlights- UT-018 preserves collagen content in in vitro collagenase challenge assays. - The Protection is UT-018 concentration-dependent across kinetic, endpoint and AUC readouts. - Preincubation of substrate with UT-018 retains protection after collagenase challenge. - The data support matrix-directed stabilization by UT-018 rather than classical active-site collagenase inhibition.

pharmacology and toxicology↗

UT-018 Accelerates Wound Repair and Hair Follicle Regeneration in Murine Models

UT-018, a stem cell chemoattractant formulation, demonstrated significant regenerative activity across independent murine wound-healing and hair-regeneration studies. Topical treatment accelerated wound closure, enhanced granulation tissue formation, improved collagen organization, increased fibroblast proliferation, and enhanced dermal vascularization. Separate hair-growth studies demonstrated increased follicular density, deeper follicular penetration, enhanced dermal vascularization, and induction of anagen-phase transition by UT-018. Mechanistic studies demonstrated strong intracellular cAMP generation and activation-associated {beta}-catenin phosphorylation consistent with GPCR-mediated regenerative signaling.

pharmacology and toxicology↗