5 research outputs found
The Practice Environment for Nurse Anesthetists in Tennessee
Potential consequences of anesthesia provider shortages may include a reduction in health care access, poor patient outcomes, and increased costs to government funded agencies. Current leaders in the anesthesia profession need to establish a work environment that is embracing, supportive, and safe so that certified registered nurse anesthetists (CRNA) can remain healthy and productive. The purpose of this Doctor of Nursing Practice (DNP) scholarly project was to provide an overview of the current CRNA practice environment in Tennessee and advocate for policies to promote CRNA retention and enhance patient access to care. The overarching goal included gathering sufficient evidence regarding the positive and negative working environments of CRNA practice and presenting this evidence to the Tennessee Association of Nurse Anesthetist (TANA) executive committee. The evidence-informed health policy model (EIHP) was used to identify the policy problem as well as guide the development, implementation, and evaluation of a solution. After reviewing the literature, project members discovered seven working environment outcomes that impact retention and patient access to care. Project members presented the seven outcomes to the TANA executive committee and distributed a pre and post presentation survey to evaluate how the TANA organization was doing at promoting a positive work environment for CRNAs. Finally, to compare and analyze the survey responses, project members ran paired sample t-tests.
Keywords: access, access to care, advanced practice registered nurse, barriers, certified registered nurse anesthetist, nurse anesthetist, and scope of practic
Insulin signaling requires glucose to promote lipid anabolism in adipocytes
Adipose tissue is essential for metabolic homeostasis, balancing lipid storage and mobilization based on nutritional status. This is coordinated by insulin, which triggers kinase signaling cascades to modulate numerous metabolic proteins, leading to increased glucose uptake and anabolic processes like lipogenesis. Given recent evidence that glucose is dispensable for adipocyte respiration, we sought to test whether glucose is necessary for insulin-stimulated anabolism. Examining lipogenesis in cultured adipocytes, glucose was essential for insulin to stimulate the synthesis of fatty acids and glyceride–glycerol. Importantly, glucose was dispensable for lipogenesis in the absence of insulin, suggesting that distinct carbon sources are used with or without insulin. Metabolic tracing studies revealed that glucose was required for insulin to stimulate pathways providing carbon substrate, NADPH, and glycerol 3-phosphate for lipid synthesis and storage. Glucose also displaced leucine as a lipogenic substrate and was necessary to suppress fatty acid oxidation. Together, glucose provided substrates and metabolic control for insulin to promote lipogenesis in adipocytes. This contrasted with the suppression of lipolysis by insulin signaling, which occurred independently of glucose. Given previous observations that signal transduction acts primarily before glucose uptake in adipocytes, these data are consistent with a model whereby insulin initially utilizes protein phosphorylation to stimulate lipid anabolism, which is sustained by subsequent glucose metabolism. Consequently, lipid abundance was sensitive to glucose availability, both during adipogenesis and in Drosophila flies in vivo. Together, these data highlight the importance of glucose metabolism to support insulin action, providing a complementary regulatory mechanism to signal transduction to stimulate adipose anabolism
Insulin signaling requires glucose to promote lipid anabolism in adipocytes.
Adipose tissue is essential for metabolic homeostasis, balancing lipid storage and mobilization based on nutritional status. This is coordinated by insulin, which triggers kinase signaling cascades to modulate numerous metabolic proteins, leading to increased glucose uptake and anabolic processes like lipogenesis. Given recent evidence that glucose is dispensable for adipocyte respiration, we sought to test whether glucose is necessary for insulin-stimulated anabolism. Examining lipogenesis in cultured adipocytes, glucose was essential for insulin to stimulate the synthesis of fatty acids and glyceride-glycerol. Importantly, glucose was dispensable for lipogenesis in the absence of insulin, suggesting that distinct carbon sources are used with or without insulin. Metabolic tracing studies revealed that glucose was required for insulin to stimulate pathways providing carbon substrate, NADPH, and glycerol 3-phosphate for lipid synthesis and storage. Glucose also displaced leucine as a lipogenic substrate and was necessary to suppress fatty acid oxidation. Together, glucose provided substrates and metabolic control for insulin to promote lipogenesis in adipocytes. This contrasted with the suppression of lipolysis by insulin signaling, which occurred independently of glucose. Given previous observations that signal transduction acts primarily before glucose uptake in adipocytes, these data are consistent with a model whereby insulin initially utilizes protein phosphorylation to stimulate lipid anabolism, which is sustained by subsequent glucose metabolism. Consequently, lipid abundance was sensitive to glucose availability, both during adipogenesis and in Drosophila flies in vivo Together, these data highlight the importance of glucose metabolism to support insulin action, providing a complementary regulatory mechanism to signal transduction to stimulate adipose anabolism