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Aalim M. Weljie

Researcher at University of Pennsylvania

Publications -  111
Citations -  6901

Aalim M. Weljie is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Metabolomics & Circadian rhythm. The author has an hindex of 41, co-authored 98 publications receiving 5749 citations. Previous affiliations of Aalim M. Weljie include University of Calgary & University of Alberta.

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Targeted profiling: quantitative analysis of 1H NMR metabolomics data.

TL;DR: The technique is validated against a traditional "spectral binning" analysis on the basis of sensitivity to water suppression, relaxation effects, and NMR spectral acquisition times using PCA pattern recognition analysis.
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Comparative metabolomics in vegans and omnivores reveal constraints on diet-dependent gut microbiota metabolite production

TL;DR: High consumption of fermentable substrate in vegans was not associated with higher levels of faecal short chain fatty acids, a finding confirmed in a 10-day controlled feeding experiment, and residence in globally distinct societies helps determine the composition of the gut microbiota that influences the production of diet-dependent gut microbial metabolites.
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Investigations of the effects of gender, diurnal variation, and age in human urinary metabolomic profiles.

TL;DR: Differences in gender, diurnal variation, and age in a human population are explored and targeted profiling produces robust models, generates accurate metabolite concentration data, and provides data that can be used to help understand metabolic differences in a healthy population.
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A branched-chain amino acid metabolite drives vascular fatty acid transport and causes insulin resistance

TL;DR: PPARGC1a is leveraged, a transcriptional coactivator that regulates broad programs of fatty acid consumption, to identify 3-hydroxyisobutyrate (3-HIB), a catabolic intermediate of the BCAA valine, as a new paracrine regulator of trans-endothelial fatty acid transport, providing a mechanistic explanation for how increased BCAA catabolic flux can cause diabetes.
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ATP-citrate lyase controls a glucose-to-acetate metabolic switch

TL;DR: It is shown that, upon genetic deletion of Acly, the gene coding for ATP-citrate lyase (ACLY), cells remain viable and proliferate, although at an impaired rate, and engagement of acetate metabolism is a crucial, although partial, mechanism of compensation for ACLY deficiency.