No abstract

OBJECTIVES:To test the hypotheses that induction of negative mood in obese binge eaters would increase food intake, and that this would be greatest in those who were highly restrained. DESIGN: Experimental manipulation of mood (neutral vs sad film) prior to the presentation of food in a taste test. PARTICIPANTS: A total of 40 obese female binge eaters (41.7 y, mean BMI ¼ 40.2 kg/m 2 ). MEASURES: Visual analogue assessment of mood and hunger motivation, dietary restraint (Dutch Eating Behaviour Questionnaire), and food intake. RESULTS: Exposure to the sad film resulted in a significant decrease in mood for both restrained and unrestrained participants. Those in the negative mood condition ate significantly more food, and the restrained eaters consumed the most. However, the expected restraint by mood interaction just failed to reach significance (P ¼ 0.06) CONCLUSIONS: The salience of negative mood in promoting overeating was confirmed. Conversely, dietary restraint had no significant impact on food intake. Further experimental work on binge eating in this group would be of value in clarifying the role of dieting and informing treatment approaches.

BBM restored cell surface GAGs and attenuated endothelial inflammation in diabetic HAECs. Blueberry might complement conventional therapies to improve vascular complications in diabetes.

Glycosaminoglycans (GAGs) are polysaccharides ubiquitously found on cell surfaces and in the extracellular matrix (ECM). They regulate numerous cellular signaling events involved in many developmental and pathophysiological processes. GAGs are composed of complex sequences of repeating disaccharide units, each of which can carry many different modifications. The tremendous structural variations account for their ability to bind many proteins and thus, for their numerous functions. Although the sequence of GAG biosynthetic events and the enzymes involved mostly were deduced a decade ago, the emergence of tissue or cell specific GAGs from a nontemplate driven process remains an enigma. Current knowledge favors the hypothesis that macromolecular assemblies of GAG biosynthetic enzymes termed "GAGOSOMEs" coordinate polymerization and fine structural modifications in the Golgi apparatus. Distinct GAG structures arise from the differential channeling of substrates through the Golgi apparatus to various GAGOSOMEs. As GAGs perform multiple regulatory roles, it is of great interest to develop molecular strategies to selectively interfere with GAG biosynthesis for therapeutic applications. In this Account, we assess our present knowledge on GAG biosynthesis, the manipulation of GAG biosynthesis using synthetic xylosides, and the unrealized potential of these xylosides in various biomedical applications. Synthetic xylosides are small molecules consisting of a xylose attached to an aglycone group, and they compete with endogenous proteins for precursors and biosynthetic enzymes to assemble GAGs. This competition reduces endogenous proteoglycan-bound GAGs while increasing xyloside-bound free GAGs, mostly chondroitin sulfate (CS) and less heparan sulfate (HS), resulting in a variety of biological consequences. To date, hundreds of xylosides have been published and the importance of the aglycone group in determining the structure of the primed GAG chains is well established. However, the structure-activity relationship has long been cryptic. Nonetheless, xylosides have been designed to increase HS priming, modified to inhibit endogenous GAG production without priming, and engineered to be more biologically relevant. Synthetic xylosides hold great promise in many biomedical applications and as therapeutics. They are small, orally bioavailable, easily excreted, and utilize the host cell biosynthetic machinery to assemble GAGs that are likely nonimmunogenic. Various xylosides have been shown, in different biological systems, to have anticoagulant effects, selectively kill tumor cells, abrogate angiogenic and metastatic pathways, promote angiogenesis and neuronal growth, and affect embryonic development. However, most of these studies utilized the commercially available one or two β-D-xylosides and focused on the impact of endogenous proteoglycan-bound GAG inhibition on biological activity. Nevertheless, the manipulation of cell behavior as a result of stabilizing growth factor signaling with xyloside-primed GAGs is also reckonable ...