Epinephrine Secretion Research Articles

MASH1 induces neuron transdifferentiation of adrenal medulla chromaffin cells.

Nerve growth factor (NGF) induces neuron transdifferentiation of adrenal medulla chromaffin cells (AMCCs) and consequently downregulates the secretion of epinephrine (EPI), which may be involved in the pathogenesis of bronchial asthma. Mammalian achaete scute-homologous 1 (MASH1), a key regulator of neurogenesis in the nervous system, has been proved to be elevated in AMCCs with neuron transdifferentiation in vivo. This study aims to explore the role of MASH1 in the process of neuron transdifferentiation of AMCCs and the mechanisms. Rat AMCCs were isolated and cultured. AMCCs were transfected with siMASH1 or MASH1 overexpression plasmid, then were stimulated with NGF and/or dexamethasone, PD98059 (a MAPK kinase-1 inhibitor) for 48 hours. Morphological changes were observed using light and electron microscope. Phenylethanolamine-N-methyltransferase (PNMT, the key enzyme for epinephrine synthesis) and tyrosine hydroxylase were detected by immunofluorescence. Western blotting was used to test the protein levels of PNMT, MASH1, peripherin (neuronal markers), extracellular regulated protein kinases (ERK), phosphorylated extracellular regulated protein kinases (pERK), and JMJD3. Real-time RT-PCR was applied to analyze the mRNA levels of MASH1 and JMJD3. EPI levels in the cellular supernatant were measured using ELISA. Cells with both tyrosine hydroxylase and PNMT positive by immunofluorescence were proved to be AMCCs. Exposure to NGF, AMCCs exhibited neurite-like processes concomitant with increases in pERK/ERK, peripherin, and MASH1 levels (all P<0.05). Additionally, impairment of endocrine phenotype was proved by a signifcant decrease in the PNMT level and the secretion of EPI from AMCCs (all P<0.01). MASH1 interference reversed the effect of NGF, causing increases in the levels of PNMT and EPI, conversely reduced the peripherin level and cell processes (all P<0.01). MASH1 overexpression significantly increased the number of cell processes and peripherin level, while decreased the levels of PNMT and EPI (all P<0.01). Compared with the NGF group, the levels of MASH1, JMJD3 protein and mRNA in AMCCs in the NGF+PD98059 group were decreased (all P<0.05). After treatment with PD98059 and dexamethasone, the effect of NGF on promoting the transdifferentiation of AMCCs was inhibited, and the number of cell processes and EPI levels were decreased (both P<0.05). In addition, the activity of the pERK/MASH1 pathway activated by NGF was also inhibited. MASH1 is the key factor in neuron transdifferentiation of AMCCs. NGF-induced neuron transdifferentiation is probably mediated via pERK/MASH1 signaling.

Benefits of IV Clonidine in Premedication on Sympathetic Hyperactivity Related to Surgical Incision

Background: Clonidine stimulates the α2 receptors of the sympathetic nervous system which have a negative presynaptic feedback effect inducing a reduction in the secretion of adrenaline and noradrenaline. The main objective of our study was to evaluate the beneficial effects of clonidine on the hemodynamic response to surgical incision. Patients and Methods: This was a prospective, single-center, randomized, single-blind clinical trial that took place over a period of 4 months in the anesthesia department of the Essos hospital center in Yaoundé. All patients over the age of 18, ASA I or II, admitted for scheduled surgery were included in the study. The patients were randomly divided into two groups by drawing lots: group A (clonidine) and group B (non-clonidine). All patients in group A received clonidine IV (3μg/kg). Heart rate, systolic blood pressure, and diastolic blood pressure were observed at different times during the surgical procedure. Results: During the study period, 35 met the inclusion criteria: 20 patients for group A and 15 patients for group B. The average age was 34 years. The sex ratio was in favor of the male gender in both groups: 2.3 in group A and 2.7 in group B. ASA class 1 was the most represented (74.3%); visceral surgery most performed of all specialties in the two groups 55% (n=11) for group A and 53% (n=8) for group B. The systolic and diastolic arterial pressure curves are parallel in the two groups. There is a slight variation in PAS and PAD in group A "clonidine" compared to the baseline values. A tendency towards systolic arterial hypertension is observed in the “non-clonidine” control group. The heart rate remains stable in group A, while tachycardia is observed at the same time for the participants in group B. Conclusion: Clonidine is an alpha 2 adrenergic receptor agonist which makes it possible to limit the hypersecretion of catecholamines, potentially deleterious for the fragile patient, at the surgical incision.

Automated Insulin Delivery for Hypoglycemia Avoidance and Glucose Counterregulation in Long-Standing Type 1 Diabetes with Hypoglycemia Unawareness.

Objective: Automated insulin delivery (AID) may benefit individuals with long-standing type 1 diabetes where frequent exposure to hypoglycemia impairs counterregulatory responses. This study assessed the effect of 18 months AID on hypoglycemia avoidance and glucose counterregulatory responses to insulin-induced hypoglycemia in long-standing type 1 diabetes complicated by impaired awareness of hypoglycemia. Methods: Ten participants mean ± standard deviation age 49 ± 16 and diabetes duration 34 ± 16 years were initiated on AID. Continuous glucose monitoring was paired with actigraphy to assess awake- and sleep-associated hypoglycemia exposure every 3 months. Hyperinsulinemic hypoglycemic clamp experiments were performed at baseline, 6, and 18 months postintervention. Hypoglycemia exposure was reduced by 3 months, especially during sleep, with effects sustained through 18 months (P ≤ 0.001) together with reduced glucose variability (P < 0.01). Results: Hypoglycemia awareness and severity scores improved (P < 0.01) with severe hypoglycemia events reduced from median (interquartile range) 3 (3-10) at baseline to 0 (0-1) events/person·year postintervention (P = 0.005). During the hypoglycemic clamp experiments, no change was seen in the endogenous glucose production (EGP) response, however, peripheral glucose utilization during hypoglycemia was reduced following intervention [pre: 4.6 ± 0.4, 6 months: 3.8 ± 0.5, 18 months: 3.4 ± 0.3 mg/(kg·min), P < 0.05]. There were increases over time in pancreatic polypeptide (Pre:62 ± 29, 6 months:127 ± 44, 18 months:176 ± 58 pmol/L, P < 0.01), epinephrine (Pre: 199 ± 53, 6 months: 332 ± 91, 18 months: 386 ± 95 pg/mL, P = 0.001), and autonomic symptom (Pre: 6 ± 2, 6 months: 6 ± 2, 18 months: 10 ± 2, P < 0.05) responses. Conclusions: AID led to a sustained reduction of hypoglycemia exposure. EGP in response to insulin-induced hypoglycemia remained defective, however, partial recovery of glucose counterregulation was evidenced by a reduction in peripheral glucose utilization likely mediated by increased epinephrine secretion and, together with improved autonomic symptoms, may contribute to the observed clinical reduction in hypoglycemia.

Nerve growth factor causes epinephrine release dysfunction by regulating phenotype alterations and the function of adrenal medullary chromaffin cells in mice with allergic rhinitis.

The presence of allergic rhinitis (AR) is an increased risk factor for the occurrence of bronchial asthma (BA). Nerve growth factor (NGF), in addition to its key role in the development and differentiation of neurons, may also be an important inflammatory factor in AR and BA. However, the pathogenesis of the progression of AR to BA remains to be elucidated. The present study aimed to investigate the ability of NGF to mediate nasobronchial interactions and explore possible underlying molecular mechanisms. In the present study, an AR mouse model was established and histology of nasal mucosa tissue injury was determined. The level of phenylethanolamine N‑methyl transferase in adrenal medulla was determined by immunofluorescence. Primary adrenal medullary chromaffin cells (AMCCs) were isolated and cultured from the adrenal medulla of mice. The expression levels of synaptophysin (SYP), STAT1, JAK1, p38 and ERK in NGF‑treated and untreated AMCCs were detected by reverse‑transcription‑quantitative PCR and western blotting. The epinephrine (EPI) and norepinephrine (NE) concentrations were measured by ELISA. It was found that the expression of SYP in AMCCs was enhanced in the presence of NGF, whereas, the concentration of EPI decreased significantly under the same conditions. Furthermore, NGF mediated the phenotypic and functional changes of AMCCs, resulting in decreased EPI secretion via JAK1/STAT1, p38 and ERK signaling. In conclusion, these findings could provide novel evidence for the role of NGF in regulating neuroendocrine mechanisms.

ISPAD Clinical Practice Consensus Guidelines 2022: Ramadan and other religious fasting by young people with diabetes.

ISPAD Clinical Practice Consensus Guidelines 2022: Ramadan and other religious fasting by young people with diabetes.

SERUM CORTISOL, PLASMA ADRENALINE AND CARDIOVASCULAR PARAMETERS MODULATION IN REGULAR PRACTICE OF YOGA IN HYPERREACTORS YOUNG HEALTHY MEDICAL STUDENTS TO COLD PRESSOR TEST.

Stress, anxiety and depression are known to be significant factors in the onset and progression of a wide spectrum of illness ranging from cardiovascular diseases, asthma, cancer, HIV-infection &amp; affect multiple systems of body. 'Almost any type of stress can greatly enhanced secretion of cortisol and adrenaline by stimulating the ACTH secretion and may be due to increased activity in the limbic system,especially in the region of the amygdala and hippocampus,The aim of this study was to investigate whether regular practice of yoga for sixty minutes twice a day for six months can improve the cardiovascular status and decrease serum cortisol and plasma adrenaline level in hyper-reactors to cold pressor test in young healthy medical students. Summary- The regular practice of yoga for six months acts as stress buster,to reduce the hyerrectivity to cold pressor test by inducing parasympathetic predominance and cortico- hypothalamo-medullary inhibition.

''CARDIOVASCULAR PARAMETERS MODULATION IN REGULAR PRACTICE OF YOGA IN HYPER-REACTORS YOUNG HEALTHY MEDICAL STUDENTS TO COLD PRESSOR TEST.”

Stress is a complex,dynamic process of interaction between a person and his or her life Stress is described as a state of anxiety, strain, nervousness, tension, constant worry or pressure, to produce hypertension and other cardiovascular disorders due to greatly enhanced secretion of cortisol and adrenaline due to increased activity in the limbic system, amygdala and hippocampus and parasympathetic predominance The aims of this study was to investigate whether regular practice of yoga for sixty minutes twice a day for six months can improve the cardiovascular parameters in hyper-reactors to cold pressor test in young healthy medical students. Summary- The regular practice of yoga for six months acts as stress buster,to reduce the hyerrectivity to cold pressor test by inducing parasympathetic predominance and cortico- hypothalamo-medullary inhibition.

Paliperidone-Induced Acute Hyperglycemia Is Caused by Adrenaline Secretion via the Activation of Hypothalamic AMP-Activated Protein Kinase.

Although paliperidone-related hyperglycemia has been extensively examined, the underlying mechanisms have not yet been elucidated. We investigated the effects of a single intravenous injection of paliperidone (0.2, 0.4, or 0.6 mg/kg) on serum concentrations of glucose and other endogenous metabolites in rats. We also examined the effects of a single intravenous injection of paliperidone (0.4 mg/kg) on AMP-activated protein kinase (AMPK) activity in the hypothalamus and liver. To clarify the relationship between AMPK activity and adrenaline secretion, the effects of berberine, which inhibits hypothalamic AMPK, on paliperidone-induced hyperglycemia were assessed. Significant increases were observed in serum glucose, adrenaline, and insulin concentrations following intravenous injections of paliperidone at doses of 0.4 and 0.6 mg/kg. A propranolol pretreatment attenuated paliperidone-induced increases in serum concentrations of glucose, but not adrenaline. Significant increases were also noted in phosphorylated AMPK concentrations in the hypothalamus following the administration of paliperidone at a dose of 0.4 mg/kg. A berberine pretreatment attenuated paliperidone-induced increases in blood concentrations of glucose, adrenaline, and insulin and phosphorylated AMPK concentrations in the hypothalamus. Collectively, the present results demonstrated that an acute treatment with paliperidone induced hyperglycemia, which was associated with the effects of hypothalamic AMPK activation on the secretion of adrenaline.

RF33 | PSUN04 Luteinizing Hormone-Chorionic Gonadotrophin Receptor in Pheochromocytomas

Abstract Background Pheochromocytomas and paragangliomas (PPGL) are catecholamine-producing neuroendocrine tumors that arise from the adrenal medulla or ganglia and display the highest heritability rate among all human tumours. Genomic analyses allowed identification of molecular subgroups of PPGL which are organized into 2 main clusters. Cluster 1 contains SDHx- and VHL-mutated tumors which do not produce epinephrine while cluster 2 includes the epinephrine-secreting PPGL related to RET, NF1, TMEM127 and MAX mutations. PPGL must be early diagnosed and treated to prevent adrenergic crises which can be life-threatening. Detection of PPGL is particularly important during pregnancy since PPGL are associated with a high risk of either maternal or fetal complications in this context. Reciprocally, pregnancy can favor adrenergic crises in patients with previously undiagnosed or silent pheochromocytoma (PCC). These dangerous events can be triggered by tumor compression resulting from fetus growth, or labor and delivery. However, it is known that surges in plasma catecholamines may also occur during early gestation suggesting that pregnancy may also activate the secretory activity of PPGL through the involvement of non-mechanical factors, such as gestational hormones. Methods In the present study, we report a case of silent PCC revealed in a pregnant woman by life-threatening adrenergic myocarditis occurring at 31 weeks of gestation. Analysis of PPGL susceptibility genes showed the presence of a heterozygous germline RET variant of uncertain significance. The fact that the first symptoms of catecholamine excess had appeared during the first trimester of pregnancy led us to conduct in vitro studies to investigate the effects of estradiol and the pregnancy hormone chorionic gonadotropin (hCG) on epinephrine secretion by cultured cells derived from the resected patient's tumor. Expression of luteinizing hormone/chorionic gonadotropin receptor (LHCGR) was searched for in the tumor and an additional series of 12 PCC by RT-qPCR and immunohistochemistry. LHCGR expression was also analyzed in silico in the PPGL cohorts of the COMETE and The Cancer Genome Atlas (TCGA) databases. Results hCG stimulated epinephrine secretion by primary cultured PCC cells. The tumor expressed the LHCG receptor, which was colocalized with catecholamine-producing enzymes. A similar expression pattern of the LHCG receptor was also observed in 5 out of a series of 12 PCCs. Moreover, in silico studies revealed that PPGL display the highest expression levels of LHCGR mRNA among the 32 solid tumor types of TCGA cohort. Interestingly, expression of LHCGR was higher in cluster 2 than in cluster 1 PPGL. Conclusion We show that PCC can express functional LHCG receptor. Consequently, pregnancy may activate catecholamine production by previously silent pheochromocytoma as early as the first trimester of gestation especially in women with gene mutations that predispose to cluster 2 epinephrine-secreting PCC. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m., Monday, June 13, 2022 1:18 p.m. - 1:23 p.m.

Synergistic augmentation of rhythmic myogenic contractions of human stomach by arginine vasopressin and adrenaline: Implications for the induction of nausea.

Nausea is associated with the hormonal secretion of vasopressin and adrenaline, although their actions in inducing nausea is poorly understood. Here, we have investigated their actions on human stomach muscle. Muscle strips were suspended in tissue baths and neuronal-/non-neuronally-mediated contractions were measured. Custom software analysed eight motility parameters defining spontaneous phasic non-neuronally mediated contractions. Receptor distributions were assessed by qPCR and immunofluorescence. V1A receptors and α1 -adrenoceptors were located on muscle as well as interstitial cells of Cajal (ICCs). Myogenic contractions of human proximal and distal stomach (respectively, 2.6 ± 0.1 and 2.7 ± 0.0 per minute; n = 44) were larger in the distal area (1.1 ± 0.1 and 5.0 ± 0.1 mN), developing relatively slowly (proximal) or rapidly (distal). Vasopressin caused tonic (proximal) or short-lived (distal) increases in muscle tone and increased myogenic contraction amplitude, frequency and rate (acting at V1A receptors; thresholds 10-11 -10-10 M); by contrast, cholinergically mediated contractions were unaffected. Oxytocin acted similarly to vasopressin but less potently, at OT receptors). Adrenaline increased (10-10 -10-5 M; α1 -adrenoceptors) and decreased (≥10-6 M; β-adrenoceptors) muscle tone and enhanced/reduced myogenic contractions. Cholinergically mediated contractions were reduced (α2 -adrenoceptors). Combined, vasopressin (10-9 M) and adrenaline (10-8 M) increased muscle tone and phasic myogenic activity in a synergistic manner. Vasopressin and adrenaline increased human gastric tone and myogenic contraction amplitude, rate of contraction and frequency. In combination, their actions were further increased in a synergistic manner. Such activity may promote nausea.

Fear conditioning as a pathogenic mechanism in the postural tachycardia syndrome.

Despite its increasing recognition and extensive research, there is no unifying hypothesis on the pathophysiology of the postural tachycardia syndrome. In this cross-sectional study, we examined the role of fear conditioning and its association with tachycardia and cerebral hypoperfusion on standing in 28 patients with postural tachycardia syndrome (31 ± 12 years old, 25 females) and 21 matched controls. We found that patients had higher somatic vigilance (P = 0.0167) and more anxiety (P < 0.0001). They also had a more pronounced anticipatory tachycardia right before assuming the upright position in a tilt-table test (P = 0.015), a physiological indicator of fear conditioning to orthostasis. While standing, patients had faster heart rate (P < 0.001), higher plasma catecholamine levels (P = 0.020), lower end-tidal CO2 (P = 0.005) and reduced middle cerebral artery blood flow velocity (P = 0.002). Multi-linear logistic regression modelling showed that both epinephrine secretion and excessive somatic vigilance predicted the magnitude of the tachycardia and the hyperventilation. These findings suggest that the postural tachycardia syndrome is a functional disorder in which standing may acquire a frightful quality, so that even when experienced alone it may elicit a fearful conditioned response. Heightened somatic anxiety is associated with and may predispose to a fear-conditioned hyperadrenergic state when standing. Our results have therapeutic implications.

Hypoglycemia: Control of counter‐regulatory hormone secretion by the brain

Hypoglycaemia is a common side‐effect of the treatment of type 1 diabetes with insulin. The Diabetes Control and Complications Trial indicated that, while intensive insulin therapy reduced the incidence and severity of diabetic complications such as retinopathy, neuropathy and nephropathy, the incidence of severe hypoglycaemia was increased 2‐3 fold. In non‐diabetic individuals, hypoglycaemia triggers the glucose counter‐regulatory response. This response consists of inhibition of insulin secretion and activation of glucagon secretion. Prolonged hypoglycaemia also evokes adrenaline secretion and less importantly, growth hormone and cortisol secretion. However, in individuals that have type 1 diabetes, the glucagon response to hypoglycaemia is lost. In these patients, the pancreatic α‐cells continue to synthesise glucagon since glucagon secretagogues such as arginine produce a robust glucagon secretory response. Our research has examined the hypothalamic and medullary neurocircuits that mediate adrenaline and glucagon secretion under conditions of neuroglucoprivation or hypoglycaemia. These studies have shown that the response to neuroglucoprivation involves specialised sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM) that mediate adrenaline secretion. These neurons are readily distinguishable from sympathetic vasomotorneurons also located in the RVLM. In addition, we have described the properties of perifornical hypothalamic (PeH) orexinergic (Ox) neurons that are activated by insulin‐induced hypoglycaemia (IHH) or neuroglucoprivation. PeH neurons project to many different targets including the RVLM and the dorsal motor nucleus of the vagus (DMV). Ox2‐R in the RVLM mediate the adrenaline secretory response. PeH neurons also mediate the glucagon response to IHH since the release of glucagon in response to IHH is diminished in Ataxin3 rats which have an age‐related loss of PeH orexin neurons.

Mechanisms of Suppression of Epinephrine Production in Rats by Low-Dose Developmental Exposure to DDT.

We studied the mechanisms underlying decreased production of epinephrine by adrenal glands in rats developmentally exposed to endocrine disruptor DDT was performed on the basis of assessment of morphology, fine structure, and function of the adrenal medulla and medullary cells. It was found that the main mechanisms of disruptive action of DDT leading to a decrease in epinephrine secretion into systemic circulation are a decrease in the growth rate of the adrenal medulla, a decrease in the number of mitochondria in adrenal cells, especially under the outer cytoplasmic membrane, destructive changes in mitochondria, and a progressive decrease in the synthesis of tyrosine hydroxylase. The decrease in the number of mitochondria and suppression tyrosine hydroxylase synthesis in adrenal cells predominate during the pubertal period, while slowdown of the growth of the adrenal medulla and progressive decrease in the synthesis of tyrosine hydroxylase seem to be the most evident mechanisms after puberty.

PD04-01 CORTISOL REGULATES ADRENALINE SYNTHESIS VIA PHENYLETHANOLAMINE N-METHYLTRANSFERASE IN SURGICAL SPECIMENS OF PHEOCHROMOCYTOMA

You have accessJournal of UrologyCME1 May 2022PD04-01 CORTISOL REGULATES ADRENALINE SYNTHESIS VIA PHENYLETHANOLAMINE N-METHYLTRANSFERASE IN SURGICAL SPECIMENS OF PHEOCHROMOCYTOMA Kazuyuki Numakura, Yuya Sekine, Yumina Muto, Mizuki Kobayashi, Soki Kashima, Ryohei Yamamoto, Atsushi Koizumi, Taketoshi Nara, Mitsuru Saito, Shintaro Narita, and Tomonori Habuchi Kazuyuki NumakuraKazuyuki Numakura More articles by this author , Yuya SekineYuya Sekine More articles by this author , Yumina MutoYumina Muto More articles by this author , Mizuki KobayashiMizuki Kobayashi More articles by this author , Soki KashimaSoki Kashima More articles by this author , Ryohei YamamotoRyohei Yamamoto More articles by this author , Atsushi KoizumiAtsushi Koizumi More articles by this author , Taketoshi NaraTaketoshi Nara More articles by this author , Mitsuru SaitoMitsuru Saito More articles by this author , Shintaro NaritaShintaro Narita More articles by this author , and Tomonori HabuchiTomonori Habuchi More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000002519.01AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Tyrosine hydroxylase (TYH), dopamine β-hydroxylase (DBH), and phenylethanolamine N-methyltransferase (PNMT) are key catecholamine synthetic enzymes (CSE) for biosynthesis from tyrosine and known for being coordinated by adrenal cortical hormones. However, little is known about the function and relationship of cortisol and CSEs for pheochromocytoma. In this study, we investigated an association between cortisol, CES, and catecholamines in pheochromocytoma patients treated by laparoscopic surgery (LA). METHODS: From September 1997 to January 2020, we performed LAs for 211 patients at the Akita University hospital. Of these, 39 patients were diagnosed with pheochromocytoma based on preoperative endocrinological evaluations and studied morning cortisol levels before surgery. Expressions of TYH, DBH, and PNMT were evaluated and classified positively by immunohistochemistry in the surgical specimens. RESULTS: The mean age of the patients was 59.0 years (range, 34–77 years; 14 men and 22 women). The mean tumor diameter was 4.3 cm (range, 1.8–8.5 cm). All laparoscopic surgeries were completed successfully. PNMT expression was very varied in individual patients (positivity: strong 17, intermediate 3, weak 7, and none 12) meanwhile, TYH and DBH were strongly expressed in all specimens. Morning cortisol value was associated with high plasma adrenaline level (correlation coefficient 0.376, p=0.034) (Figure 1). Additionally, patients with strong PNMT expression showed higher adrenaline level in both plasma (0.30 ng/ml vs 0.03 ng/ml, p=0.005) and urine (87.9 μg/day vs 21.1 μg/day, p=0.038) (Table 1). CONCLUSIONS: Cortisol secretion is positively related to adrenaline levels in pheochromocytoma patients. Strong PNMT expression is associated with a high level of adrenaline secretion. Thus, cortisol might regulate catecholamine synthesis via PNMT. Source of Funding: None © 2022 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 207Issue Supplement 5May 2022Page: e48 Advertisement Copyright & Permissions© 2022 by American Urological Association Education and Research, Inc.MetricsAuthor Information Kazuyuki Numakura More articles by this author Yuya Sekine More articles by this author Yumina Muto More articles by this author Mizuki Kobayashi More articles by this author Soki Kashima More articles by this author Ryohei Yamamoto More articles by this author Atsushi Koizumi More articles by this author Taketoshi Nara More articles by this author Mitsuru Saito More articles by this author Shintaro Narita More articles by this author Tomonori Habuchi More articles by this author Expand All Advertisement PDF DownloadLoading ...

Impact of Prenatal and Postnatal Exposure to Endocrine Disrupter DDT on Adrenal Medulla Function

Epinephrine is the most abundant catecholamine hormone, produced by the nervous system and adrenal glands. Endocrine disruption of epinephrine synthesis, secretion and signaling is less studied than steroid and thyroid hormones. Dichlorodiphenyltrichloroethane (DDT) is recognized as one of the most prominent environmental contaminants with a long half-life. It is a potent endocrine disrupter affecting sex steroid, mineralocorticoid, glucocorticoid and thyroid hormone production. Exposure to low doses of DDT is universal and begins in utero. Therefore, we studied adrenal medulla growth and function in male Wistar rats exposed to low doses of DDT during prenatal and postnatal development until puberty and adulthood, as well as rats exposed to DDT since the first day of postnatal development. All the exposed rats demonstrated lowered epinephrine blood levels, gradually reducing with age. DDT was found to inhibit the synthesis of tyrosine hydroxylase and affect the mitochondrial apparatus of epinephrine-producing cells during puberty and even after maturation. Low-dose exposure to DDT from birth resulted in more pronounced changes in adrenomedullary cells and a more profound decrease (up to 50%) in epinephrine secretion in adult rats. Prenatal onset of exposure demonstrated a mild effect on epinephrine-producing function (30% reduction), but was associated with lower rate of adrenal medulla growth during maturation and 25% smaller adrenal medullar size in adult rats. All subjects exposed to low doses of DDT failed to develop adaptive changes and restore proper epinephrine production. These results indicate a dysmorphogenetic effect of prenatal exposure and disruption of secretory function of adrenal chromaffin cells by postnatal exposure to DDT.

HUBUNGAN KECEMASAN TERHADAP KUALITAS TIDUR MAHASISWA BARU PRODI FISIOTERAPI UNIVERSITAS BALI INTERNASIONAL

The problem that occurs in new students is anxiety. This anxiety can be caused by changes in the social environment. This change in situation causes uncertainty which will lead to increased secretion of adrenaline. Academic problems such as study load can be another factor for students experiencing anxiety. When someone feels anxious, there will be an increase in the hormones cortisol, epinephrine, and norepinephrine which is affect the central nervous system, causing a state of wakefulness and increasing alertness in the central nervous system. This will make it difficult for students to start sleeping and cause poor sleep quality. This study aims to determine the relationship between anxiety and sleep quality in the new students in Prodi Fisioterapi Universitas Bali Internasional. This study used a cross sectional study design. The sampling technique used is the total sampling for 29 people. The research was conducted at the Program Studi Fisioterapi Universitas Bali Internasional in December 2021. Measurement of sleep quality using PSQI (Pittsburgh Sleep Quality Index) and anxiety measured using HSR-A (Hemiilton Rating Scale for Anxiety). Data were analyzed with SPSS 23.0, using the chi square test. The results between anxiety and sleep quality is p=0,001 (p&lt;0,05), which means that there is a significant relationship between anxiety and sleep quality in new students.

Suprarenal cortical extract against adrenal insufficiency (Addison's disease)

Contrary to the generally accepted view that Addison's disease develops as a result of insufficient epinephrine secretion by the adrenal medulla Rogoff and Stewart (A. MA, 1929, 11 / V) see the cause of this disease in the insufficiency of the adrenal cortex. The product interrenalin isolated from this layer, which was used by the authors on dogs with removed adrenal glands and on patients with Addison's disease, gave extremely favorable results. Interrenaline was administered intravenously to dogs, per os in humans. The authors cite 7 case histories where, after the administration of this drug, the symptoms of Addison's disease improved or disappeared: blood pressure increased, bronze color disappeared, gastrointestinal disorders stopped and weakness disappeared, etc.

Effects of dexmedetomidine on glucose-related hormones and lactate in non-diabetic patients under general anesthesia: a randomized controlled trial

The aim of this study was to explore the effects of dexmedetomidine on glucose-related hormones and lactate levels in non-diabetic patients undergoing malignant gastrointestinal tumor radical resection. Groups D<inf>1</inf> and D<inf>2</inf> received dexmedetomidine loading dose 1 µg/kg and maintenance dose 0.25 and 0.5 µg/kg/h, respectively. Group C received saline solution. Glucose, lactate, insulin, glucagon, cortisol, epinephrine, norepinephrine and dopamine levels were measured before dexmedetomidine infusion (T<inf>1</inf>), 1 h after surgery beginning (T<inf>2</inf>), at surgery ending (T<inf>3</inf>), and 1 h after transfer to the postanesthesia care unit (T<inf>4</inf>). Compared with group C, glucose levels increased in group D<inf>2</inf> at T<inf>2</inf> and reduced in groups D<inf>1</inf> and D<inf>2</inf> at T<inf>4</inf>. Lactate levels reduced in groups D<inf>1</inf> and D<inf>2</inf> at T<inf>4</inf>. A positive correlation between glucose and lactate levels was found in all groups. Compared with group C, insulin level reduced in group D<inf>2</inf> at T<inf>2</inf>; glucagon levels reduced in groups D<inf>1</inf> and D<inf>2</inf> at T<inf>4</inf>; cortisol levels reduced in group D<inf>1</inf> at T<inf>4</inf> and in group D<inf>2</inf> at T<inf>3</inf> and T<inf>4</inf>; epinephrine and norepinephrine levels reduced in group D<inf>1</inf> at T<inf>4</inf> and in group D<inf>2</inf> at T<inf>2</inf> and T<inf>4</inf>; and dopamine level reduced in group D<inf>2</inf> at T<inf>4</inf>. Dexmedetomidine loading dose 1 µg/kg and maintenance dose 0.25 µg/kg/h produces a stable insulin level and significant postoperative decreases in glucagon, cortisol, epinephrine and norepinephrine secretion with stable maintenance of intraoperative and postoperative blood glucose levels and decreased postoperative lactate levels in non-diabetic patients under general anesthesia.

Advances in the Molecular Genetics of Catecholaminergic Polymorphic Ventricular Tachycardia.

Catecholaminergic polymorphic ventricular tachycardia is a primary arrhythmogenic syndrome with genetic features most commonly seen in adolescents, with syncope and sudden death following exercise or agitation as the main clinical manifestations. The mechanism of its occurrence is related to the aberrant release of Ca2+ from cardiomyocytes caused by abnormal RyR2 channels or CASQ2 proteins under conditions of sympathetic excitation, thus inducing a delayed posterior exertional pole, manifested by sympathetic excitation inducing adrenaline secretion, resulting in bidirectional or polymorphic ventricular tachycardia. The mortality rate of the disease is high, but patients usually do not have organic heart disease, the clinical manifestations may not be obvious, and no significant abnormal changes in the QT interval are often observed on electrocardiography. Therefore, the disease is often easily missed and misdiagnosed. A number of genetic mutations have been linked to the development of this disease, and the mechanisms are different. In this paper, we would like to summarize the possible genes related to catecholaminergic polymorphic ventricular tachycardia in order to review the genetic tests currently performed, and to further promote the development of genetic testing techniques and deepen the research on the molecular level of this disease.

Intestinal microbiota modulates adrenomedullary response through Nod1 sensing in chromaffin cells

SummaryThe intestinal microbiota closely interacts with the neuroendocrine system and exerts profound effects on host physiology. Here, we report that nucleotide-binding oligomerization domain 1 (Nod1) ligand derived from intestinal bacteria modulates catecholamine storage and secretion in mouse adrenal chromaffin cells. The cytosolic peptidoglycan receptor Nod1 is involved in chromogranin A (Chga) retention in dense core granules (DCGs) in chromaffin cells. Mechanistically, upon recognizing its ligand, Nod1 localizes to DCGs, and recruits Rab2a, which is critical for Chga and epinephrine retention in DCGs. Depletion of Nod1 ligand or deficiency of Nod1 leads to a profound defect in epinephrine storage in chromaffin cells and subsequently less secretion upon stimulation. The intestine-adrenal medulla cross talk bridged by Nod1 ligand modulates adrenal medullary responses during the immobilization-induced stress response in mice. Thus, our study uncovers a mechanism by which intestinal microbes modulate epinephrine secretion in response to stress, which may provide further understanding of the gut-brain axis.