Angela Subauste
University of Mississippi Medical Center
26 Papers
181 Citations
Angela Subauste is an academic researcher from University of Mississippi Medical Center. The author has contributed to research in topics: Diabetes mellitus & Medicine. The author has an hindex of 14, co-authored 25 publications. Previous affiliations of Angela Subauste include University of Michigan & University of Mississippi.
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Papers
Roux-En-Y Gastric Bypass Vs. Sleeve Gastrectomy: Balancing the Risks of Surgery with the Benefits of Weight Loss.
Corey J. Lager,Nazanene H. Esfandiari,Angela Subauste,Andrew T. Kraftson,Morton B. Brown,Ruth Cassidy,Catherine K. Nay,Amy L. Lockwood,Oliver A. Varban,Elif A. Oral +9 more
TL;DR: Weight loss was greater following Roux-en-Y gastric bypass compared to SG at 2 years and the risk for surgical complications was greaterFollowing GB, suggesting that surgical intervention should be tailored to surgical risk, comorbidities, and desired weight loss.
Diabetic muscle infarction: a systematic review
TL;DR: A combination of bed rest, glycemic control, and non-steroidal anti-inflammatory drug therapy appears to yield the shortest time to symptom resolution and the lowest risk of recurrence.
90
Alterations in lipid signaling underlie lipodystrophy secondary to AGPAT2 mutations.
Angela Subauste,Arun K. Das,Xiangquan Li,Brandon Elliot,Charles R. Evans,Mahmoud A. El Azzouny,Mary K. Treutelaar,Elif A. Oral,Todd Leff,Charles F. Burant +9 more
TL;DR: It is concluded that AGPAT2 regulates adipogenesis through the modulation of the lipome, altering normal activation of phosphatidylinositol 3-kinase (PI3K)/Akt and PPARγ pathways in the early stages of adipogenesis.
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DGAT: novel therapeutic target for obesity and type 2 diabetes mellitus.
TL;DR: Recent studies have shown that mice deficient in this enzyme are resistant to diet induced obesity and have increased insulin and leptin sensitivity, suggesting that inhibition of DGAT in vivo may be a novel therapeutic target not only for obesity but also for diabetes.
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Role of CD40-dependent down-regulation of CD154 in impaired induction of CD154 in CD4(+) T cells from HIV-1-infected patients.
TL;DR: This work identifies CD40 as a mediator of impaired CD154 induction in HIV-1 infection and explains why this defect was not detected by studies where T cell activation was triggered independently of CD40+ APCs.