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Long Beach, United States

Gelberg H.A.,1301 Wilshire Blvd. | Kwan C.L.,1301 Wilshire Blvd. | Mena S.J.,1301 Wilshire Blvd. | Erickson Z.D.,1301 Wilshire Blvd. | And 6 more authors.
Eating Behaviors | Year: 2015

Weight gain and worsening metabolic parameters are often side effects of antipsychotic medications used by individuals with severe mental illness. To address this, a randomized, controlled research study of a behavioral weight management program for individuals with severe mental illness was undertaken to assess its efficacy. Patients unable to meet weight loss goals during the first portion of the year-long study were given the option of using meal replacement shakes in an effort to assist with weight loss. Specific requirements for use of meal replacement shakes were specified in the study protocol; only five patients were able to use the shakes in accordance with the protocol and lose weight while improving metabolic parameters. Case studies of two subjects are presented, illustrating the challenges and obstacles they faced, as well as their successes. Taking responsibility for their own weight loss, remaining motivated through the end of the study, and incorporating the meal replacement shakes into a daily routine were factors found in common with these patients. Use of meal replacements shakes with this population may be effective. © 2015. Source


O'Mahony F.,901 East 7th Street | O'Mahony F.,University of California at Irvine | O'Mahony F.,Royal College of Surgeons in Ireland | Razandi M.,901 East 7th Street | And 6 more authors.
Molecular Endocrinology | Year: 2012

Most cancers use glucose as substrate for aerobic glycolysis in preference to oxidative phosphorylation. However, variable glucose concentrations within the in-vivo tumor microenvironment may necessitate metabolic plasticity. Furthermore, little information exists on a role for estrogen receptors in modulating possible metabolic adaptations in breast cancer cells. Here we find that MCF-7 cells switch between metabolic pathways depending on glucose availability and 17β-estradiol (E2) potentiates adaptation. In high glucose conditions E2 up-regulates glycolysis via enhanced AKT kinase activity and suppresses tricarboxylic acid cycle activity. After a decrease in extracellular glucose, mitochondrial pathways are activated in preference to glycolysis. In this setting, E2 suppresses glycolysis and rescues cell viability by stimulating the tricarboxylic acid cycle via the up-regulation of pyruvate dehydrogenase (PDH) activity. E2 also increases ATP in low glucose-cultured cells, and the novel phosphorylation of PDH by AMP kinase is required for these metabolic compensations. Capitalizing on metabolic vulnerability, knockdown of PDH in the low-glucose state strongly potentiates ionizing radiationinduced apoptosis and reverses the cell survival effects of E2. We propose that lowering glucose substrate and inhibiting PDH may augment adjuvant therapies for estrogen receptor-positive breast cancer. © 2012 by The Endocrine Society. Source

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