ORCID Profile
0000-0001-7994-110X
Current Organisations
University of Toronto
,
University Health Network
,
Krembil Research Institute
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Publications
Restricting Branched-Chain Amino Acids within a High-Fat Diet Prevents Obesity
Publisher: MDPI AG
Date: 07-04-2022
Abstract: Obesity is a global pandemic, but there is yet no effective measure to control it. Recent metabolomics studies have identified a signature of altered amino acid profiles to be associated with obesity, but it is unclear whether these findings have actionable clinical potential. The aims of this study were to reveal the metabolic alterations of obesity and to explore potential strategies to mitigate obesity. We performed targeted metabolomic profiling of the plasma/serum s les collected from six independent cohorts and conducted an in idual data meta-analysis of metabolomics for body mass index (BMI) and obesity. Based on the findings, we hypothesized that restriction of branched-chain amino acids (BCAAs), phenylalanine, or tryptophan may prevent obesity and tested our hypothesis in a dietary restriction trial with eight groups of 4-week-old male C57BL/6J mice (n = 5/group) on eight different types of diets, respectively, for 16 weeks. A total of 3397 in iduals were included in the meta-analysis. The mean BMI was 30.7 ± 6.1 kg/m2, and 49% of participants were obese. Fifty-eight metabolites were associated with BMI and obesity (all p ≤ 2.58 × 10−4), linked to alterations of the BCAA, phenylalanine, tryptophan, and phospholipid metabolic pathways. The restriction of BCAAs within a high-fat diet (HFD) maintained the mice’s weight, fat and lean volume, subcutaneous and visceral adipose tissue weight, and serum glucose and insulin at levels similar to those in the standard chow group, and prevented obesity, adipocyte hypertrophy, adipose inflammation, and insulin resistance induced by HFD. Our data suggest that four metabolic pathways, BCAA, phenylalanine, tryptophan, and phospholipid metabolic pathways, are altered in obesity and restriction of BCAAs within a HFD can prevent the development of obesity and insulin resistance in mice, providing a promising strategy to potentially mitigate diet-induced obesity.
The role of antioxidants in models of inflammation: Emphasis on l-arginine and arachidonic acid metabolism
Publisher: Springer Science and Business Media LLC
Date: 2005
DOI: 10.1163/156856005774382797
Abstract: Inflammatory processes are made up of a multitude of complex cascades. Under physiological conditions these processes aid in tissue repair. However, under pathophysiological environments, such as wound healing and hypoxia-ischaemia (HI), inflammatory mediators become imbalanced, resulting in tissue destruction. This review addresses the changes in reactive oxygen species (ROS), L-arginine and arachidonic acid metabolism in wound healing and HI and subsequent treatments with promising anti-oxidants. Even though these models may appear ergent, anti-oxidant treatments are nevertheless still having favourable effects. On the basis of recent findings, it is apparent that protection with anti-oxidants is not solely attributed to scavenging of ROS. In addition, the actions of anti-oxidants must be considered in light of the inflammatory process being assessed. To this end, there does not appear to be any universally applicable single mechanism to explain the actions of anti-oxidants.
Loss of peroxisome proliferator–activated receptor γ in mouse fibroblasts results in increased susceptibility to bleomycin‐induced skin fibrosis
Publisher: Wiley
Date: 27-08-2009
DOI: 10.1002/ART.24761
Abstract: There is increasing evidence that the transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma) plays an important role in controlling cell differentiation, and that PPARgamma ligands can modify inflammatory and fibrotic responses. The aim of the present study was to examine the role of PPARgamma in a mouse model of skin scleroderma, in which mice bearing a fibroblast-specific deletion of PPARgamma were used. Cutaneous sclerosis was induced by subcutaneous injection of bleomycin, while untreated control groups were injected with phosphate buffered saline. Mice bearing a fibroblast-specific deletion of PPARgamma were investigated for changes in dermal thickness, inflammation, collagen content, and the number of alpha-smooth muscle actin-positive cells. The quantity of the collagen-specific amino acid hydroxyproline was also measured. In addition, the effect of PPARgamma deletion on transforming growth factor beta1 (TGFbeta1) signaling in the fibroblasts was investigated. Bleomycin treatment induced marked cutaneous thickening and fibrosis in all treated mice. Deletion of PPARgamma resulted in enhanced susceptibility to bleomycin-induced skin fibrosis, as indicated by increases in all measures of skin fibrosis and enhanced sensitivity of fibroblasts to TGFbeta1 in PPAR-deficient mice. These results indicate that PPARgamma suppresses fibrogenesis. Specific agonists of PPARgamma may therefore alleviate the extent of the development of cutaneous sclerosis.
mPGES-1 null mice are resistant to bleomycin-induced skin fibrosis
Publisher: Springer Science and Business Media LLC
Date: 2011
DOI: 10.1186/AR3226
Related Organisations
Sheffield Hallam University
Location: United Kingdom of Great Britain and Northern Ireland
Related Funding Activities
No related grants have been discovered for Mohit Kapoor.