Collectively, this study sheds light on the chemosensory functions of the liver and unveils potentially important regulators of hepatic homeostasis.Stac3 regulates excitation-contraction coupling (EC coupling) in vertebrate skeletal muscles by regulating the L-type voltage-gated calcium channel (Cav channel). Recently a stac-like gene, Dstac, was identified in Drosophila and found to be expressed by both a subset of neurons and muscles. Here, we show that Dstac and Dmca1D, the Drosophila L-type Cav channel, are necessary for normal locomotion by larvae.  https://www.selleckchem.com/products/kpt-330.html  Immunolabeling with specific antibodies against Dstac and Dmca1D found that Dstac and Dmca1D are expressed by larval body-wall muscles. Furthermore, Ca2+ imaging of muscles of Dstac and Dmca1D deficient larvae found that Dstac and Dmca1D are required for excitation-contraction coupling. Finally, Dstac appears to be required for normal expression levels of Dmca1D in body-wall muscles. These results suggest that Dstac regulates Dmca1D during EC coupling and thus muscle contraction.Phospholipids (PL) are essential molecules for larval growth and development. In this study, growth, lipid metabolism and gene expression responses associated with different dietary PL levels in pelagic sole larvae were evaluated. In a first trial, the long-term effects on growth and survival of two experimental microdiets (MD) containing high (High-PL) or low (Low-PL) PL levels were tested and compared to a diet based on live prey (rotifers). The MD were supplied from 3 to 10 days post-hatch (dph) and Artemia from day 8 to 29 dph. High-PL fed larvae had higher dry mass (1.2-fold) than Low-PL fed larvae at 8 dph and both MD were smaller (2.9-fold) than larvae fed live preys. However, a compensatory growth (33% between 8 and 20 dph) occurred when MD were substituted by Artemia and by the end of the trial no significant differences in mass or survival occurred between the dietary treatments. In a second trial, growth, lipid metabolism and gene expression profiles of larvae fed with MD up to 8 dph were analyzed. Growth data confirmed that mass of larvae fed with High-PL was higher (1.3-fold) than the those fed Low-PL and they had lower levels of triacylglycerol (2.8-fold), cholesterol (1.2-fold) and cetoleic acid (1.7-fold). Histological analysis indicated an excess of lipid vacuoles in larvae fed with Low-PL and the expression analysis revealed a coordinated response to enhance lipid mobilization since the expression of genes involved in PL intermediate synthesis, PL remodeling as well as eight apolipoprotein was up-regulated. The down-regulation of apolipoprotein apob2 in larvae fed with Low-PL indicated a specific regulation by PL levels. The present work provides insight into the responses associated with dietary PL in early fish larvae, which will be of use for future studies aimed as designing effective larval sole diets.Our understanding of cerebral blood flow (CBF) regulation during functional activation is still limited. Alongside with the accepted role of smooth muscle cells in controlling the arteriolar diameter, a new hypothesis has been recently formulated suggesting that CBF may be modulated by capillary diameter changes mediated by pericytes. In this study, we developed in vitro microvascular network models featuring a valve enabling the dilation of a specific micro-channel. This allowed us to investigate the non-uniform red blood cell (RBC) partitioning at microvascular bifurcations (phase separation) and the hematocrit distribution at rest and for two scenarios modeling capillary and arteriolar dilation. RBC partitioning showed similar phase separation behavior during baseline and activation. Results indicated that the RBCs at diverging bifurcations generally enter the high-flow branch (classical partitioning). Inverse behavior (reverse partitioning) was observed for skewed hematocrit profiles in the parent vessel of bifurcations, especially for high RBC velocity (i.e., arteriolar activation). Moreover, results revealed that a local capillary dilation, as it may be mediated in vivo by pericytes, led to a localized increase of RBC flow and a heterogeneous hematocrit redistribution within the whole network. In case of a global increase of the blood flow, as it may be achieved by dilating an arteriole, a homogeneous increase of RBC flow was observed in the whole network and the RBCs were concentrated along preferential pathways. In conclusion, overall increase of RBC flow could be obtained by arteriolar and capillary dilation, but only capillary dilation was found to alter the perfusion locally and heterogeneously.Northern elephant seals (NES, Mirounga angustirostris) undergo an annual molt during which they spend ∼40 days fasting on land with reduced activity and lose approximately one-quarter of their body mass. Reduced activity and muscle load in stereotypic terrestrial mammalian models results in decreased muscle mass and capacity for force production and aerobic metabolism. However, the majority of lost mass in fasting female NES is from fat while muscle mass is largely preserved. Although muscle mass is preserved, potential changes to the metabolic and contractile capacity are unknown. To assess potential changes in NES skeletal muscle during molt, we collected muscle biopsies from 6 adult female NES before the molt and after ∼30 days at the end of the molt. Skeletal muscle was assessed for respiratory capacity using high resolution respirometry, and RNA was extracted to assess changes in gene expression. Despite a month of reduced activity, fasting, and weight loss, skeletal muscle respiratory capacity was preserved with no change in OXPHOS respiratory capacity. Molt was associated with 162 upregulated genes including those favoring lipid metabolism. We identified 172 downregulated genes including those coding for ribosomal proteins and genes associated with skeletal muscle force transduction and glucose metabolism. Following ∼30 days of molt, NES skeletal muscle metabolic capacity is preserved although mechanotransduction may be compromised. In the absence of exercise stimulus, fasting-induced shifts in muscle metabolism may stimulate pathways associated with preserving the mass and metabolic capacity of slow oxidative muscle.