Ali Aminian, Andrea Zelisko, John P Kirwan+2 more · 2015 · Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery · Elsevier · added 2026-04-24
Low HDL cholesterol is an independent cardiac risk factor. A general efficacy gradient exists for the resolution of cardiovascular risk factors after bariatric surgery (i.e., biliopancreatic diversion Show more
Low HDL cholesterol is an independent cardiac risk factor. A general efficacy gradient exists for the resolution of cardiovascular risk factors after bariatric surgery (i.e., biliopancreatic diversion [BPD]>Roux-en-Y gastric bypass [RYGB]>sleeve gastrectomy [SG]>adjustable gastric banding [AGB]). However, a review of high level of evidence clinical studies shows a different hierarchy for the effect of bariatric surgery on HDL (i.e., RYGB=SG>BPD, AGB). Surgically induced weight loss effectively reverses many steps in HDL metabolism that have been altered with obesity. Furthermore, enterocytes contribute to HDL levels through the synthesis of apolipoproteins A-IV and A-I. RYGB and SG that preserve the small intestine (particularly the jejunum) lead to a significant rise in HDL. However, when the small intestinal contribution does not reinforce the weight loss dependent mechanisms (e.g., after BPD and AGB), only a modest rise in HDL occurs. Further experimental and clinical studies are required to better delineate the issue. Show less
Integrin-containing focal adhesions transmit extracellular signals across the plasma membrane to modulate cell adhesion, signalling and survival. Although integrins are known to undergo continuous end Show more
Integrin-containing focal adhesions transmit extracellular signals across the plasma membrane to modulate cell adhesion, signalling and survival. Although integrins are known to undergo continuous endo/exocytic traffic, the potential impact of endocytic traffic on integrin-induced signals is unknown. Here, we demonstrate that integrin signalling is not restricted to cell-ECM adhesions and identify an endosomal signalling platform that supports integrin signalling away from the plasma membrane. We show that active focal adhesion kinase (FAK), an established marker of integrin-ECM downstream signalling, localizes with active integrins on endosomes. Integrin endocytosis positively regulates adhesion-induced FAK activation, which is early endosome antigen-1 and small GTPase Rab21 dependent. FAK binds directly to purified endosomes and becomes activated on them, suggesting a role for endocytosis in enhancing distinct integrin downstream signalling events. Finally, endosomal integrin signalling contributes to cancer-related processes such as anoikis resistance, anchorage independence and metastasis. Show less