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Biology subjects

McEntee, K.

Publications and source records attributed to McEntee, K..

2 recordsLinked to original sources

Body condition score and triglyceride concentrations and their associations with other markers of energy homeostasis in healthy, non-obese dogs

Serum triglyceride concentrations increase in dogs in overweight condition, which is typically assessed by body condition score (BCS). However, their associations with other markers of energy homeostasis are poorly characterized. The present study aimed to evaluate the associations between both BCS and triglyceride levels and other markers of lipid and glucose metabolism in healthy dogs in overweight condition. 534 overweight, but otherwise healthy, client-owned dogs were included. Serum concentrations of cholesterol, free fatty acids, triglycerides, insulin, glucose and fructosamine were measured. Dogs were assigned to lean (BCS: 3-5) or overweight (BCS: 6-7) categories, and linear models were used to assess the differences between BCS categories and the associations between triglycerides and the other variables, correcting for the effect of breed. Globally, "overweight" dogs had greater serum cholesterol (95% CI: 5.3-6.2 mmol/L or 205-237 mg/dL versus 5.1-5.4 mmol/L or 198-210 mg/dl, P = .003), insulin (95% CI: 17.5-22.1 U/ml versus 16.7-18.0 U/ml, P = .036) and were older (95% CI: 4.0-5.3 versus 3.4-3.7 years, P = .002) than lean dogs. Triglyceride concentrations were positively associated with fructosamine (r2 = 0.31, P = .001), cholesterol (r2 = 0.25, P < .001), insulin (r2 = 0.14, P = .003) and glucose (r2 = 0.10, P = .002), and negatively associated with free fatty acids (r2 = 0.11, P < .001). There was no association between triglyceride levels and age. In conclusion, both BCS and triglyceride concentrations were associated with other markers of glucose and lipid metabolism in overweight, but otherwise healthy dogs. Triglyceride concentrations were associated with an increase in insulin and fructosamine that might reflect an early-phase impairment in glucose tolerance which, surprisingly, was concurrent with lower basal free fatty acids.

physiology↗

Activation of Smad 2/3 signaling by low shear stress mediates artery inward remodeling

RationaleBlood vessel remodeling in response to changes in tissue demand is an important aspect of fitness and is often compromised in vascular disease. Endothelial cell (EC) sensing of fluid shear stress (FSS) governs vessel remodeling to maintain FSS at a specific magnitude or set point in healthy vessels.\n\nObjectiveThe purpose of this study was to understand how shear stress-regulated Smad 2/3 contributes to artery remodeling.\n\nMethods and ResultsWe found that shear stress induces Smad 2/3 phosphorylation, nuclear translocation, and gene expression in ECs. Nuclear translocation and gene expression are maximal at low and decrease at high FSS. Reducing flow in the mouse carotid by ligation of branch vessels induces Smad2 nuclear localization in vivo. Activation of Smad 2/3 by FSS requires the Type I TGF{beta} family receptor Alk5 and the transmembrane protein Neuropilin-1. Flow activation of Smad 2/3 is mediated by increased sensitivity to BMP9 but not BMP10 or TGF{beta}. By contrast, flow activation of Smad 1/5 is maximal at physiological FSS and requires BMP9 or 10 binding to Alk1 and Endoglin. EC-specific deletion of Alk5 in mice blocks low flow-induced inward remodeling after carotid ligation.\n\nConclusionsTogether, these data elucidate a novel pathway that mediates low flow-induced inward artery remodeling. These results may be relevant to inward remodeling in diseased vessels where Smad 2/3 is activated by pathological stimuli.

cell biology↗