Reductive stress in mitochondria isolated from the carotid body of type 1 diabetic male Wistar rats.

The carotid body (CB) senses changes in arterial O partial pressure (pO) and glucose levels; therefore, it is key for the detection of hypoxia and hypoglycemia. The CB has been suggested to detect pO through an increase in reactive oxygen species (ROS) in the mitochondria. However, the mechanism protecting the chemoreceptor cells and their mitochondria from ROS and hyperglycemia is poorly understood.

Hybrid lineages of CD4 T cells: a handbook update.

CD4 T lymphocytes have been classified into several lineages, according to their gene expression profiles and their effector responses. Interestingly, recent evidence is showing that many lineages could yield hybrid phenotypes with unique properties and functions. It has been reported that such hybrid lineages might underlie pathologies or may function as effector cells with protection capacities against molecular threats.

K252a Prevents Microglial Activation Induced by Anoxic Stimulation of Carotid Bodies in Rats.

Inducing carotid body anoxia through the administration of cyanide can result in oxygen deprivation. The lack of oxygen activates cellular responses in specific regions of the central nervous system, including the Nucleus Tractus Solitarius, hypothalamus, hippocampus, and amygdala, which are regulated by afferent pathways from chemosensitive receptors. These receptors are modulated by the brain-derived neurotrophic factor receptor TrkB.

Molecular tracking of insulin resistance and inflammation development on visceral adipose tissue.

Background: Visceral adipose tissue (VAT) is one of the most important sources of proinflammatory molecules in obese people and it conditions the appearance of insulin resistance and diabetes. Thus, understanding the synergies between adipocytes and VAT-resident immune cells is essential for the treatment of insulin resistance and diabetes.

Methods: We collected information available on databases and specialized literature to construct regulatory networks of VAT resident cells, such as adipocytes, CD4+ T lymphocytes and macrophages.

Leptin in the Commissural Nucleus of the Tractus Solitarius (cNTS) and Anoxic Stimulus in the Carotid Body Chemoreceptors Increases cNTS Leptin Signaling Receptor and Brain Glucose Retention in Rats.

: The commissural nucleus of the tractus solitarius (cNTS) not only responds to glucose levels directly, but also receives afferent signals from the liver, and from the carotid chemoreceptors (CChR). In addition, leptin, through its receptors in the cNTS, regulates food intake, body weight, blood glucose levels, and brain glucose retention (BGR). These leptin effects on cNTS are thought to be mediated through the sympathetic-adrenal system.

Moderate and high intensity chronic exercise reduces plasma tumor necrosis factor alpha and increases the Langerhans islet area in healthy rats.

Objective: This study aimed to examine the effects of moderate (MIT) and high-intensity training (HIT) chronic exercise on plasma tumor necrosis factor alpha (TNF-α) level and its impact on Langerhans islet morphology in healthy rats.

Methods: Two-month old normal male Wistar rats were divided into three groups: control (C, n=6), MIT (n=6), and HIT (n=4). The training protocol consisted in 24 sessions of running on a treadmill at 60-80% maximal oxygen consumption (VO) for MIT, and >80% VO for HIT.

Leptin in the Commissural Nucleus Tractus Solitarii Increases the Glucose Responses to Carotid Chemoreceptors Activation by Cyanide.

Leptin is a protein hormone that plays a key role in the regulation of energy balance and glucose homeostasis. Leptin and all leptin receptor isoforms are present in the carotid bodies, but its precise function in glucose regulation and metabolism is not yet known. The aim of this study was to determine whether exogenous leptin, microinjected into the commissural nucleus tractus solitarii (cNTS), preceding sodium cyanide (NaCN) injection into the circulatory isolated carotid sinus (ICS), in vivo, modifies hyperglycemic reflex (HR) and brain glucose retention (BGR).

Nitric oxide in the nucleus of the tractus solitarius is involved in hypoglycemic conditioned response.

The repeated injection of insulin (unconditioned stimulus, UCS) immediately followed by exposure to sensory stimulation (e.g. sound or odor; conditioned stimulus, CS) results in a learned conditioned reflex in which the exposure to the CS alone lowers blood glucose.

Effect of moderate and high intensity chronic exercise on the pancreatic islet morphometry in healthy rats: BDNF receptor participation.

The function and morphology of β-cells is largely dependent on insulin demand. As β-cells cover a bigger cell proportion in pancreas islets, changes of insulin producer cells affect the whole pancreatic islet morphology. Growth factors as the neurotrophins regulate the pancreas physiology, besides; physical exercise increases insulin sensitivity, and further modifies brain derived neurotrophic factor (BDNF) concentration in plasma.

Effects of moderate- and high-intensity chronic exercise on brain-derived neurotrophic factor expression in fast and slow muscles.

Introduction: Brain-derived neurotrophic factor (BDNF) protein expression is sensitive to cellular activity. In the sedentary state, BDNF expression is affected by the muscle phenotype.

Methods: Eighteen Wistar rats were divided into the following 3 groups: sedentary (S); moderate-intensity training (MIT); and high-intensity training (HIT).

Chronic exercise increases plasma brain-derived neurotrophic factor levels, pancreatic islet size, and insulin tolerance in a TrkB-dependent manner.

Background: Physical exercise improves glucose metabolism and insulin sensitivity. Brain-derived neurotrophic factor (BDNF) enhances insulin activity in diabetic rodents. Because physical exercise modifies BDNF production, this study aimed to investigate the effects of chronic exercise on plasma BDNF levels and the possible effects on insulin tolerance modification in healthy rats.

Nitric oxide in the commissural nucleus tractus solitarii regulates carotid chemoreception hyperglycemic reflex and c-Fos expression.

Carotid body chemoreceptors function as glucose sensors and contribute to glucose homeostasis. The nucleus tractus solitarii (NTS) is the first central nervous system (CNS) nuclei for processing of information arising in the carotid body. Here, we microinjected a nitric oxide (NO) donor sodium nitroprusside (SNP), an NO-independent activator of the soluble guanylyl cyclase (sGC) (YC₁) or an NO-synthase (NOS) inhibitor Nω-nitro-l-arginine methyl ester (L-NAME) into the commissural NTS (cNTS) before carotid chemoreceptor anoxic stimulation and measured arterial glucose and the expression of Fos-like immunoreactivity (Fos-ir).

Brain-derived neurotrophic factor in the nucleus tractus solitarii modulates glucose homeostasis after carotid chemoreceptor stimulation in rats.

Neuronal systems, which regulate energy intake, energy expenditure and endogenous glucose production, sense and respond to input from hormonal related signals that convey information from body energy availability. Carotid chemoreceptors (CChr) function as sensors for circulating glucose levels and contribute to glycemic counterregulatory responses. Brain-derived neurotrophic factor (BDNF) that plays an important role in the endocrine system to regulate glucose metabolism could play a role in hyperglycemic glucose reflex with brain glucose retention (BGR) evoked by anoxic CChr stimulation.

Concomitant effects of nitric oxide and carotid chemoreceptor stimulation on brain glucose in normoglycemic and hyperglycemic rats.

Background And Aims: Carotid body (CB) sinus perfusion with different glucose concentrations modifies arterial glucose concentration and brain glucose retention, thereby changing the brain's threshold to hypoxia. Because nitric oxide (NO) modulates hypoxic chemoreception, we investigated the relationship between NO- and CB-receptor pathways on arterial glucose and brain arteriovenous (a-v) glucose difference after hypoxic stimulation under hyperglycemic conditions.

Methods: Normoglycemic and streptozotocin (STZ, 50 mg/kg i.

GabaB receptors activation in the NTS blocks the glycemic responses induced by carotid body receptor stimulation.

The carotid body receptors participate in glucose regulation sensing glucose levels in blood entering the cephalic circulation. The carotid body receptors information, is initially processed within the nucleus tractus solitarius (NTS) and elicits changes in circulating glucose and brain glucose uptake. Previous work has shown that gamma-aminobutyric acid (GABA) in NTS modulates respiratory reflexes, but the role of GABA within NTS in glucose regulation remains unknown.

Carotid chemoreceptor reflex modulation by arginine-vasopressin microinjected into the nucleus tractus solitarius in rats.

Background: In addition to their role of sensing O2, pH, CO2, osmolarity and temperature, carotid body receptors (CBR) were proposed by us and others to have a glucose-sensing role in the blood entering the brain, integrating information about blood glucose and O2 levels essential for central nervous system (CNS) metabolism. The nucleus tractus solitarius (NTS) is an important relay station in central metabolic control and receives signals from peripheral glucose-sensitive hepatoportal afferences, from central glucose-responsive neurons in the brainstem and from CBR and arginine-vasopressin (AVP)-containing axons from hypothalamic nuclei.

Methods: In normal Wistar rats anesthetized with pentobarbital, permanent cannulas were placed stereotaxically in the NTS.

Induction of brain glucose uptake by a factor secreted into cerebrospinal fluid.

It is well established that the carotid body receptors (CBR), at the bifurcation of the carotid artery, inform the brain of changes in the concentration of CO(2) and O(2) in arterial blood. More recent work suggests that these receptors are also extremely sensitive to blood glucose levels suggesting that they may play an important role as sensors of blood components important for brain energy metabolism. Much less is known about changes in brain glucose metabolism in response to CBR activation.