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1.
Clinical Approach to Sodium Homeostasis Disorders in Children with Pituitary-Suprasellar Tumors.
Tuli, G, Matarazzo, P, de Sanctis, L
Neuroendocrinology. 2020;(3-4):161-171
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Abstract
Children with pituitary-suprasellar tumors are at high risk of developing sodium metabolism disorders since the tumoral mass itself or surgical and medical treatment can damage AVP release circuits. Additional risk factors are represented by the use of hypotonic fluids, the young age, total parenteral nutrition, and obstructive hydrocephalus secondary to tumor pathology. The most frequent hyponatremic disorders related to AVP in these patients are the syndrome of inappropriate ADH secretion and the cerebral/renal salt wasting syndrome, while hypernatremic conditions include central diabetes insipidus (CDI) and adipsic CDI. The main challenge in the management of these patients is to promptly distinguish the AVP release disorder at the base of the sodium imbalance and treat it correctly by avoiding rapid sodium fluctuations. These disorders can coexist or follow each other in a few hours or days; therefore, careful clinical and biochemical monitoring is necessary, especially during surgery, the use of chemotherapeutic agents, or radiotherapy. This monitoring should be performed by experienced healthcare professionals and should be multidisciplinary, including pediatric endocrinologists, neurosurgeons, and oncologists since maintaining sodium homeostasis also plays a prognostic role in terms of disease survival, therapeutic response, hospitalization rate, and mortality. In this review, we analyze the management of sodium homeostasis disorders in children with pituitary-suprasellar tumors and discuss the main challenges in the diagnosis and treatment of these conditions based on literature data and over 30 years of clinical experience at our Department of Pediatric Endocrinology.
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The Role of Autophagy in Liver Epithelial Cells and Its Impact on Systemic Homeostasis.
Tomaipitinca, L, Mandatori, S, Mancinelli, R, Giulitti, F, Petrungaro, S, Moresi, V, Facchiano, A, Ziparo, E, Gaudio, E, Giampietri, C
Nutrients. 2019;(4)
Abstract
: Autophagy plays a role in several physiological and pathological processes as it controls the turnover rate of cellular components and influences cellular homeostasis. The liver plays a central role in controlling organisms' metabolism, regulating glucose storage, plasma proteins and bile synthesis and the removal of toxic substances. Liver functions are particularly sensitive to autophagy modulation. In this review we summarize studies investigating how autophagy influences the hepatic metabolism, focusing on fat accumulation and lipids turnover. We also describe how autophagy affects bile production and the scavenger function within the complex homeostasis of the liver. We underline the role of hepatic autophagy in counteracting the metabolic syndrome and the associated cardiovascular risk. Finally, we highlight recent reports demonstrating how the autophagy occurring within the liver may affect skeletal muscle homeostasis as well as different extrahepatic solid tumors, such as melanoma.
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The effects of coenzyme Q10 administration on glucose homeostasis parameters, lipid profiles, biomarkers of inflammation and oxidative stress in patients with metabolic syndrome.
Raygan, F, Rezavandi, Z, Dadkhah Tehrani, S, Farrokhian, A, Asemi, Z
European journal of nutrition. 2016;(8):2357-2364
Abstract
BACKGROUND Limited data are available indicating the effects of coenzyme Q10 (CoQ10) supplementation on metabolic status of patients with metabolic syndrome (MetS). PURPOSE The present study was conducted to determine the effects of CoQ10 administration on glucose homeostasis parameters, lipid profiles, biomarkers of inflammation and oxidative stress among patients with MetS. METHODS This randomized, double-blind, placebo-controlled trial was performed among 60 overweight or obese and type 2 diabetes mellitus patients with coronary heart disease aged 40-85 years old. Participants were randomly allocated into two groups. Group A (n = 30) received 100 mg CoQ10 supplements and group B (n = 30) received placebo for 8 weeks. Fasting blood samples were taken at the beginning of the study and after 8-week intervention to quantify glucose homeostasis parameters, lipid profiles and biomarkers of inflammation and oxidative stress. RESULTS Compared with the placebo, CoQ10 supplementation resulted in a significant reduction in serum insulin levels (-2.1 ± 7.1 vs. +4.1 ± 7.8 µIU/mL, P = 0.002) and homeostasis model of assessment-insulin resistance (-0.7 ± 2.1 vs. +1.0 ± 2.0, P = 0.002) and homeostatic model assessment-beta cell function (-5.9 ± 22.2 vs. +15.9 ± 34.0, P = 0.005). In addition, patients who received CoQ10 supplements had a significant increase in plasma total antioxidant capacity (TAC) concentrations (+26.0 ± 105.0 vs. -162.2 ± 361.8 mmol/L, P = 0.008) compared with the placebo group. However, after adjustment for the baseline levels, age and baseline BMI, the effect on TAC levels (P = 0.08) disappeared. Additionally, compared with the placebo group, a significant positive trends in plasma glutathione (P = 0.06) and a significant reduction in malondialdehyde (P = 0.08) were seen among patients who received CoQ10 supplement. We did not observe any significant changes in fasting plasma glucose, lipid concentrations and inflammatory markers. CONCLUSIONS Overall, daily intake of 100 mg CoQ10 supplements among patients with MetS for 8 weeks had beneficial effects on serum insulin levels, HOMA-IR, HOMA-B and plasma TAC concentrations. CLINICAL TRIAL REGISTRATION NUMBER www.irct.ir : IRCT201502245623N35.
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Quantifying phenotypic flexibility as the response to a high-fat challenge test in different states of metabolic health.
Kardinaal, AF, van Erk, MJ, Dutman, AE, Stroeve, JH, van de Steeg, E, Bijlsma, S, Kooistra, T, van Ommen, B, Wopereis, S
FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 2015;(11):4600-13
Abstract
Metabolism maintains homeostasis at chronic hypercaloric conditions, activating postprandial response mechanisms, which come at the cost of adaptation processes such as energy storage, eventually with negative health consequences. This study quantified the metabolic adaptation capacity by studying challenge response curves. After a high-fat challenge, the 8 h response curves of 61 biomarkers related to adipose tissue mass and function, systemic stress, metabolic flexibility, vascular health, and glucose metabolism was compared between 3 metabolic health stages: 10 healthy men, before and after 4 wk of high-fat, high-calorie diet (1300 kcal/d extra), and 9 men with metabolic syndrome (MetS). The MetS subjects had increased fasting concentrations of biomarkers representing the 3 core processes, glucose, TG, and inflammation control, and the challenge response curves of most biomarkers were altered. After the 4 wk hypercaloric dietary intervention, these 3 processes were not changed, as compared with the preintervention state in the healthy subjects, whereas the challenge response curves of almost all endocrine, metabolic, and inflammatory processes regulating these core processes were altered, demonstrating major molecular physiologic efforts to maintain homeostasis. This study thus demonstrates that change in challenge response is a more sensitive biomarker of metabolic resilience than are changes in fasting concentrations.
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The islet circadian clock: entrainment mechanisms, function and role in glucose homeostasis.
Rakshit, K, Qian, J, Colwell, CS, Matveyenko, AV
Diabetes, obesity & metabolism. 2015;(0 1):115-22
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Abstract
Circadian regulation of glucose homeostasis and insulin secretion has long been appreciated as an important feature of metabolic control in humans. Circadian disruption is becoming increasingly prevalent in today's society and is likely responsible in part for the considerable rise in type 2 diabetes (T2DM) and metabolic syndrome worldwide. Thus, understanding molecular mechanisms driving the inter-relationship between circadian disruption and T2DM is important in context of disease prevention and therapeutics. In this regard, the goal of this article is to highlight the role of the circadian system, and islet circadian clocks in particular, as potential regulators of β-cell function and survival. To date, studies have shown that islet clocks respond to changes in feeding patterns, and regulate a multitude of critical cellular processes in insulin secreting β-cells (e.g. insulin exocytosis, mitochondrial function and response to oxidative stress). Subsequently, either genetic or environmental disruption of normal islet clock performance compromises β-cell function and leads to loss of glycaemic control. Future work is warranted to further unravel the role of circadian clocks in human islet function in health and contributions to pathogenesis of T2DM.
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Fat sensing and metabolic syndrome.
Youn, JH
Reviews in endocrine & metabolic disorders. 2014;(4):263-75
Abstract
Overconsumption of dietary fat contributes to the development of obesity and metabolic syndrome. Recent evidence suggests that high dietary fat may promote these metabolic states not only by providing calories but also by inducing impaired control of energy balance. In normal metabolic states, fat interacts with various organs or receptors to generate signals for the regulation of energy balance. Many of these interactions are impaired by high-fat diets or in obesity, contributing to the development or maintenance of obesity. These impairments may arise largely from fundamental alterations in the hypothalamus where all peripheral signals are integrated to regulate energy balance. This review focuses on various mechanisms by which fat is sensed at different stages of ingestion, circulation, storage, and utilization to regulate food intake, and how these individual mechanisms are altered by high-fat diets or in obesity.
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Egg intake during carbohydrate restriction alters peripheral blood mononuclear cell inflammation and cholesterol homeostasis in metabolic syndrome.
Andersen, CJ, Lee, JY, Blesso, CN, Carr, TP, Fernandez, ML
Nutrients. 2014;(7):2650-67
Abstract
Egg yolk contains bioactive components that improve plasma inflammatory markers and HDL profiles in metabolic syndrome (MetS) under carbohydrate restriction. We further sought to determine whether egg yolk intake affects peripheral blood mononuclear cell (PBMC) inflammation and cholesterol homeostasis in MetS, as HDL and its associated lipid transporter ATP-binding cassette transporter A1 (ABCA1) reduce the inflammatory potential of leukocytes through modulation of cellular cholesterol content and distribution. Thirty-seven men and women classified with MetS consumed a moderate carbohydrate-restricted diet (25%-30% of energy) for 12 weeks, in addition to consuming either three whole eggs per day (EGG) or the equivalent amount of yolk-free egg substitute (SUB). Interestingly, lipopolysaccharide-induced PBMC IL-1β and TNFα secretion increased from baseline to week 12 in the SUB group only, despite increases in PBMC toll-like receptor 4 (TLR4) mRNA expression in the EGG group. Compared to baseline, ABCA1 and 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase mRNA expression increased by week 12 in the EGG group only, whereas changes in PBMC total cholesterol positively correlated with changes in lipid raft content. Together, these findings suggest that intake of whole eggs during carbohydrate restriction alters PBMC inflammation and cholesterol homeostasis in MetS.
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A prospective study of glucose homeostasis in quetiapine-treated schizophrenic patients by using the intravenous glucose tolerance test.
Chen, CH, Lin, TY, Chen, TT, Chen, VC, Lin, NC, Shao, WC, Lu, ML
Progress in neuro-psychopharmacology & biological psychiatry. 2011;(4):965-9
Abstract
Increasing attention has been paid recently to the potential diabetogenic effect of second-generation antipsychotics (SGAs). The objective of this prospective study was to evaluate the effects of quetiapine treatment on pancreatic beta-cell function in SGA-naïve schizophrenic patients. Seventeen schizophrenic subjects completed an eight-week trial. The metabolic parameters were assessed at weeks 0, 2, 4, and 8. We measured glucose homeostasis with the intravenous glucose tolerance test. After the eight-week treatment, body weight and body mass index showed to be significantly increased compared to those at baseline. No significant changes were found in serum levels of fasting glucose, insulin, total cholesterol, and high-density lipoprotein. Insulin resistance and insulin secretion were significantly increased. Incidences of clinically significant weight gain and treatment-emergent metabolic syndrome were 11.8% and 11.8%, respectively. This study result confirms the association of quetiapine treatment and impairment of glucose homeostasis in schizophrenic patients.
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Peroxisome proliferator-activated receptor: effects on nutritional homeostasis, obesity and diabetes mellitus.
Viana Abranches, M, Esteves de Oliveira, FC, Bressan, J
Nutricion hospitalaria. 2011;(2):271-9
Abstract
The obesity and the metabolic disorders associated characterize the metabolic syndrome, which has increased at an alarming rate around the world. It is known that environmental and genetic factors are involved in the genesis of obesity. Peroxisome Proliferator-Activated Receptors (PPARs) stand out among these factors. They compose the nuclear receptor superfamily and there are in three isoforms (PPARα,PPARβ/δ and PPARγ), which play an important role in the regulation of the metabolism of carbohydrates, lipids and proteins. The present review aims to understand the relationship between the diet, the PPARs and the control of the blood glucose and body weight, since the understanding about the mechanisms by which these receptors act may benefit the development of the strategies aiming at prevention and elaboration of therapeutics actions which are more effective for the treatment of obesity and diabetes.
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[The influence of antihypertensive agents on plasmatic and vascular-thrombocytic homeostasis in metabolic syndrome].
Vengerovskiĭ, AI, Idrisova, EM, Bushkova, EA, Mananko, EI, Krasnova, NM
Eksperimental'naia i klinicheskaia farmakologiia. 2008;(6):8-12
Abstract
The combined therapy with enalapril and prolonged-release verapamil, as well as with enalapril and moxonidine significantly increases the level of antiatherogenic high-density-lipoprotein cholesterol, reduces the atherogenicity coefficients, decreases the concentrations of glucose, glycosylated hemoglobin, and soluble fibrinmonomeric complexes and the aggregation activity of thrombocytes, activates plasminogen in the blood of patients under conditions of metabolic syndrome with arterial hypertension. At the same time the enalapril monotherapy has no significant influence on the parameters of lipid and carbohydrate metabolism and the plasmatic and vascular-thrombocytic homeostasis.