Biology subjects

Bedard, A.

Publications and source records attributed to Bedard, A..

3 recordsLinked to original sources

bioRxiv2025

The evolution of cavefish odor perception shifts fish response from avoidance to approach when exposed to alarm and death odors.

An organisms survival is dependent on activating the correct behavioral circuit in response to a stimulus. While stimulus perception is largely conserved, we still do not know the evolutionary mechanisms that drive changes in stimulus perception. Therefore, we wondered how odor perception has evolved in cavefish that encounter vastly different odors compared to their surface ancestors. While surface populations show attraction to social odors and avoidance of alarm and death odors, cave populations are sexually dimorphic in their responses to social odors and exhibit attraction to alarm and death odors. Finally, we find that odor perception variation is genetically encoded and plastic, while tissue clearing and brain mapping suggest odor perception is governed by thalamic and hypothalamic circuits. Taken together, we describe a unique model for investigating the environmental, genetic, and neurological mechanisms underlying olfactory evolution in vertebrates.

evolutionary biology↗

bioRxiv2025

Cholesterol Metabolism in a Murine Model of Vertical Sleeve Gastrectomy

The most effective and durable treatment for obesity is metabolic bariatric surgery. Currently, vertical sleeve gastrectomy (VSG) has become the preferred surgical method to achieve sustained weight loss and reverse obesity-related disease, including dyslipidemias. Human studies indicate that 40% of VSG patients can discontinue statin treatment by 6 months, while alterations in plasma bile acids and synthesis have been observed after bariatric surgery. Although it is well known that cholesterol is the precursor for all bile acids, the link between changes in plasma cholesterol and bile acids remains unclear in the context of VSG. Here, we present a murine model of VSG that leads to a marked decrease in plasma cholesterol levels despite no difference in body weight compared to sham surgery. Our results demonstrate that gastric resection lowers systemic cholesterol burden by promoting the hepatobiliary elimination of cholesterol through the upregulation of bile acid synthesis. These observations imply that gastric resection impacts overall hepatic physiology and cholesterol homeostasis independent of weight loss.

physiology↗

bioRxiv2018

Toll-Like Receptor-4 Disruption Suppresses Adipose Tissue Remodeling and Increases Survival During Cancer Cachexia Syndrome

Cancer-induced cachexia, characterized by systemic inflammation, body weight loss, adipose tissue (AT) remodeling and muscle wasting, is a malignant metabolic syndrome with undefined etiology. Here, we show that Toll-like receptor 4 (TLR4) mediates AT remodeling, in particular, AT browning and inflammatory response in mice bearing Lewis lung carcinoma (LLC). LLC tumor-bearing (TB) TLR4-/- mice were spared from AT remodeling due to a reduced macrophage infiltration and adipocyte atrophy. TLR4-/- mice were also resistant to cold-induced browning of subcutaneous AT (scAT). Importantly, pharmacological inhibition of TLR4 reproduced the main protective effect against AT remodeling found in TLR4-/- TB mice. Moreover, the treatment was effective in prolonging the survival and attenuating tumor mass growth when compared to non-treated-TB animals. Further, tumor-induced elevation of circulating pro-inflammatory cytokines was similarly abolished in both genetic ablation and pharmacological inhibition of TLR4. These data suggest that TLR4 is a critical mediator and a promising therapeutic target for cancer-induced AT remodeling.\n\nHIGHLIGHTSO_LIGenetic ablation and pharmacological inhibition of TLR4 attenuate adipose tissue remodeling during cancer-associated cachexia;\nC_LIO_LITLR4 suppression play an essential role in the browning phenotype induced by cachexia;\nC_LIO_LIAdministration of TLR4 drug inhibitor increase survival and reduces tumor mass growth in tumor bearing mice;\nC_LIO_LITLR4 pathway is a promising target for cancer-cachexia therapeutic intervention.\nC_LI

cancer biology↗