scholarly journals Mitochondria as target of endocrine-disrupting chemicals: implications for type 2 diabetes

2018 ◽  
Vol 239 (2) ◽  
pp. R27-R45 ◽  
Author(s):  
Laura Marroqui ◽  
Eva Tudurí ◽  
Paloma Alonso-Magdalena ◽  
Iván Quesada ◽  
Ángel Nadal ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Mitochondrial Dysfunction ◽  
Energy Homeostasis ◽  
Hormone Secretion ◽  
Endocrine Disrupting Chemicals ◽  
Oxidative Capacity ◽  
Endocrine Disrupting ◽  
Diabetes Development

Type 2 diabetes is a chronic, heterogeneous syndrome characterized by insulin resistance and pancreatic β-cell dysfunction or death. Among several environmental factors contributing to type 2 diabetes development, endocrine-disrupting chemicals (EDCs) have been receiving special attention. These chemicals include a wide variety of pollutants, from components of plastic to pesticides, with the ability to modulate endocrine system function. EDCs can affect multiple cellular processes, including some related to energy production and utilization, leading to alterations in energy homeostasis. Mitochondria are primarily implicated in cellular energy conversion, although they also participate in other processes, such as hormone secretion and apoptosis. In fact, mitochondrial dysfunction due to reduced oxidative capacity, impaired lipid oxidation and increased oxidative stress has been linked to insulin resistance and type 2 diabetes. Herein, we review the main mechanisms whereby metabolism-disrupting chemical (MDC), a subclass of EDCs that disturbs energy homeostasis, cause mitochondrial dysfunction, thus contributing to the establishment of insulin resistance and type 2 diabetes. We conclude that MDC-induced mitochondrial dysfunction, which is mainly characterized by perturbations in mitochondrial bioenergetics, biogenesis and dynamics, excessive reactive oxygen species production and activation of the mitochondrial pathway of apoptosis, seems to be a relevant mechanism linking MDCs to type 2 diabetes development.

Endocrine Disruptors and the Induction of Insulin Resistance.

2020 ◽  
Vol 16 ◽  
Author(s):  
Rafael Vanni ◽  
Renata Maksoud Bussuan ◽  
Renato Luiz Rombaldi ◽  
Alberto K. Arbex
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Endocrine Disruptors ◽  
Large Scale ◽  
Endocrine Disrupting Chemicals ◽  
Insulin Resistance Syndrome ◽  
Public Health Care ◽  
Scale Production ◽  
Endocrine Disrupting

Introduction: The incidence of insulin resistance syndrome and type 2 diabetes mellitus has increased at an alarming rate worldwide and constitutes a serious challenge to public health care in the 21st century. Endocrine disrupting chemicals are defined as “substances or mixtures of substances that alter the endocrine system function[s] and, hence, adversely affect organisms, their progeny, or [sub] populations” and may be associated with this increase in prevalence. Objective: This study aimed to assess the role of endocrine disrupting chemicals in insulin resistance and the importance of approaching the subject during anamnesis. Methods: A full review of the literature regarding insulin resistance, type-2 diabetes and endocrine disruptors was conducted. Conclusion: Large-scale production and distribution of endocrine disrupting chemicals coincide with the increase in prevalence of insulin resistance globally. In recent years, studies have shown that endocrine disrupting chemicals are positively associated with insulin resistance syndrome, evidenced by worse prognoses among individuals with higher levels of exposure. Health professionals should recognize the forms of exposure, most susceptible people, and lifestyle habits that can worsen patients’ prognoses.

scholarly journals Insulin Resistance (IR) in Patients with Type 2 Diabetes Mellitus. Identifying Predictors of Insulin Resistance and Establishing a Correlation Between Insulin Resistance and Cardiovascular Risk

2018 ◽  
Vol 15 (2) ◽  
pp. 7-15
Author(s):  
Vesa Cosmin Mihai ◽  
Popa Loredana ◽  
Daina Lucia ◽  
Moisi Mădălina ◽  
Popescu Mircea ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Cardiovascular Risk ◽  
Biochemical Parameters ◽  
Diabetes Development ◽  
Effect Of Age ◽  
Determinant Factor

AbstractInsulin resistance is a determinant factor for the increased prevalence of hypertension and dyslipidemia in type 2 diabetes patients. In this study we determined those modifications of clinical and biochemical parameters associated with insulin resistance in the diabetic patient, these alterations can offer us indications concerning the pathophysiological mechanisms that lead to the diabetes development in the case of most patients. Also we determined a correlation between insulin resistance and cardiovascular risk, through the combined effect of age and insulin resistance on this risk.

scholarly journals Relationship Between Oxidative Stress, ER Stress, and Inflammation in Type 2 Diabetes: The Battle Continues

2019 ◽  
Vol 8 (9) ◽  
pp. 1385 ◽  
Author(s):  
Burgos-Morón ◽  
Abad-Jiménez ◽  
Marañón ◽  
Iannantuoni ◽  
Escribano-López ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Current Knowledge ◽  
Β Cells ◽  
The Relationship ◽  
And Oxidative Stress

Type 2 diabetes (T2D) is a metabolic disorder characterized by hyperglycemia and insulin resistance in which oxidative stress is thought to be a primary cause. Considering that mitochondria are the main source of ROS, we have set out to provide a general overview on how oxidative stress is generated and related to T2D. Enhanced generation of reactive oxygen species (ROS) and oxidative stress occurs in mitochondria as a consequence of an overload of glucose and oxidative phosphorylation. Endoplasmic reticulum (ER) stress plays an important role in oxidative stress, as it is also a source of ROS. The tight interconnection between both organelles through mitochondrial-associated membranes (MAMs) means that the ROS generated in mitochondria promote ER stress. Therefore, a state of stress and mitochondrial dysfunction are consequences of this vicious cycle. The implication of mitochondria in insulin release and the exposure of pancreatic β-cells to hyperglycemia make them especially susceptible to oxidative stress and mitochondrial dysfunction. In fact, crosstalk between both mechanisms is related with alterations in glucose homeostasis and can lead to the diabetes-associated insulin-resistance status. In the present review, we discuss the current knowledge of the relationship between oxidative stress, mitochondria, ER stress, inflammation, and lipotoxicity in T2D.

scholarly journals Sex differences in the effects of androgens acting in the central nervous system on metabolism

2016 ◽  
Vol 18 (4) ◽  
pp. 415-424 ◽  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Central Nervous System ◽  
Nervous System ◽  
Metabolic Regulation ◽  
Energy Homeostasis ◽  
Sexually Dimorphic ◽  
Metabolic Homeostasis ◽  
The Central Nervous System

One of the most sexually dimorphic aspects of metabolic regulation is the bidirectional modulation of glucose and energy homeostasis by testosterone in males and females. Testosterone deficiency predisposes men to metabolic dysfunction, with excess adiposity, insulin resistance, and type 2 diabetes, whereas androgen excess predisposes women to insulin resistance, adiposity, and type 2 diabetes. This review discusses how testosterone acts in the central nervous system, and especially the hypothalamus, to promote metabolic homeostasis or dysfunction in a sexually dimorphic manner. We compare the organizational actions of testosterone, which program the hypothalamic control of metabolic homeostasis during development, and the activational actions of testosterone, which affect metabolic function after puberty. We also discuss how the metabolic effect of testosterone is centrally mediated via the androgen receptor.

scholarly journals РОЛЬ МАРКЕРА КОСТНОГО РЕМОДЕЛИРОВАНИЯ ОСТЕОКАЛЬЦИНА В РЕГУЛЯЦИИ ЭНЕРГЕТИЧЕСКОГО ГОМЕОСТАЗА ПРИ САХАРНОМ ДИАБЕТЕ 2 ТИПА

World Science ◽  
2020 ◽  
Vol 2 (5(57)) ◽  
pp. 20-29
Author(s):  
Ковальчук А. В. ◽  
Зиныч О. В. ◽  
Корпачев В. В. ◽  
Кушнарева Н. Н. ◽  
Прибила О. В.
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Energy Homeostasis ◽  
Visceral Obesity ◽  
Mineral Density ◽  
General Group ◽  
Men And Women ◽  
Visceral Adipose

Osteocalcin (OK) is actively involved in the humoral regulation of energy homeostasis. However, the relationship between the level of OK as a modulator of metabolic processes and constitutional and metabolic features in patients with type 2 diabetes mellitus (DM) of a different gender remains not thoroughly studied.The study included 127 patients with type 2 diabetes ≥ 50 years of age. Of these, 70 were postmenopausal women and 57 men.It was found that in the general group of women, the concentration of OK in the blood serum was significantly higher than in men. The observed difference is due to significantly higher levels of OK in women of the older age group (≥ 60 years) in comparison with men. At the same time, a decrease in bone mineral density (BMD) in the femoral neck was observed in subgroups of men and women aged ≥ 60 years and older, while in the younger subgroups of patients, the BMD of lumbar and femoral zones were close to each other.The relationships between OK levels and adipose tissue parameters, evaluated by calculating the morphological and functional index of visceral obesity (IVO), were investigated. An increase in the OK level in the groups of men and women was accompanied by a decrease in the IVO values. The highest degree of insulin resistance was determined in groups of patients with minimal levels of OK and high IVO, and the lowest values were recorded in patients with high levels of OK and low IVO.The decrease of the blood OK level in patients with type 2 diabetes occurs in parallel with an increase in the degree of insulin resistance and dysfunction of visceral adipose tissue. In this case, IVO is a more accurate parameter reflecting the constitutional and metabolic phenotypic changes, compared with the index of the waist circumference. The decrease in BMD in patients with type 2 diabetes is the result of predominantly involutive processes that are noticeable at the age of ≥ 60 years and occur against the background of a decrease in the content of OK with age.

scholarly journals Resumen de Conferencias

2018 ◽  
Vol 5 (2) ◽  
pp. 5-33
Author(s):  
Asociación Colombiana de Endocrinología Diabetes y Metabolismo
Keyword(s):  
Type 2 Diabetes ◽  
Thyroid Cancer ◽  
Endocrine Disrupting Chemicals ◽  
Duration Of Treatment ◽  
Endocrine Disrupting ◽  
Síndrome Metabólico ◽  
Non Coding Rnas

Listado Conferencia Hipotiroidismo congénito: ¿qué se afecta además de la tiroides? . Raúl Calzada León Conferencia La etapa fetal extrauterina. Raúl Calzada León Conferencia Mecanismos del síndrome de resistencia a hormonas tiroideas (RTH). Guillermo Juvenal Conferencia Diagnóstico y tratamiento del hipopituitarismo. Karina Danilowicz Conferencia Deficiencia combinada de hormonas hipofisiarias. Karina Danilowicz Conferencia Melatonina, GH y trastornos metabólicos. Hugo Fideleff Conferencia Etapa de transición: una visión crítica. Hugo Fideleff Conferencia Tiroides y fertilidad. Marcos Abalovich Conferencia Síndromes hereditarios de tumores hipofisarios. Moisés Mercado Conferencia Impacto metabólico en la fertilidad del varón. Roald Gómez Pérez Conferencia Tratamiento del exoftalmos. Alicia Gauna Conferencia Terapias orientadas a la lesión metastásica en carcinoma diferenciado de tiroides. Inés Califano Conferencia Cirugía bariátrica y metabólica. César Ernesto Guevara Pérez Conferencia Endocrine disrupting chemicals, estrogen and epigenetics. Jon Entine Conferencia Insuficiencia renal y osteoporosis. Salomón Jasqui Conferencia Rebote adiposo temprano y riesgo cardiometabólico futuro: edad de inicio vs. persistencia de la obesidad. Raquel Burrows Conferencia Hasta dónde debemos tener en cuenta consideraciones de economía de la salud en nuestra práctica clínica. Juan José Gagliardino Conferencia ¿Estamos listos para implementar programas de prevención primaria en Latinoamérica? Pablo Aschner Conferencia Ginecomastia. Pablo Knoblovits (Argentina) Conferencia La disfunción eréctil en el síndrome metabólico. Pablo Knoblovits Conferencia Hiperaldosteronismo primario. Alejandro Román González, Carlos Alfonso Builes-Barrera Conferencia Obesidad, efectos ambientales y compuestos químicos. Fernando Lizcano Conferencia Microcarcinoma papilar de tiroides y vigilancia activa. Hernán Tala Conferencia The old and new times in treatment for osteoporosis? What medication for whom, sequence and duration of treatment?.  Michael McClung Conferencia Diabetes, osteoporosis and obesity: are they related?  Michael McClung, MD Conferencia Deregulation of non-coding Rnas in thyroid cancer. Alfredo Fusco, Pierlorenzo Pallante, Romina Sepe, Simona Pellecchia, Marco De Martino, Francesco Esposito, Alfredo Fusco Conferencia The new understanding of type 2 diabetes - simplicity revealed. Roy Taylor. Professor of Medicine and Metabolism, Newcastle University, UK

scholarly journals Mitochondrial Function in Skeletal Muscle Is Normal and Unrelated to Insulin Action in Young Men Born with Low Birth Weight

2008 ◽  
Vol 93 (10) ◽  
pp. 3885-3892 ◽  
Author(s):  
Charlotte Brøns ◽  
Christine B. Jensen ◽  
Heidi Storgaard ◽  
Amra Alibegovic ◽  
Stine Jacobsen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Young Men ◽  
Hepatic Insulin Resistance

Objective: Low birth weight (LBW) is an independent risk factor of insulin resistance and type 2 diabetes. Recent studies suggest that mitochondrial dysfunction and impaired expression of genes involved in oxidative phosphorylation (OXPHOS) may play a key role in the pathogenesis of insulin resistance in aging and type 2 diabetes. The aim of this study was to determine whether LBW in humans is associated with mitochondrial dysfunction in skeletal muscle. Methods: Mitochondrial capacity for ATP synthesis was assessed by 31phosphorus magnetic resonance spectroscopy in forearm and leg muscles in 20 young, lean men with LBW and 26 matched controls. On a separate day, a hyperinsulinemic euglycemic clamp with excision of muscle biopsies and dual-energy x-ray absorptiometry scanning was performed. Muscle gene expression of selected OXPHOS genes was determined by quantitative real-time PCR. Results: The LBW subjects displayed a variety of metabolic and prediabetic abnormalities, including elevated fasting blood glucose and plasma insulin levels, reduced insulin-stimulated glycolytic flux, and hepatic insulin resistance. Nevertheless, in vivo mitochondrial function was normal in LBW subjects, as was the expression of OXPHOS genes. Conclusions: These data support and expand previous findings of abnormal glucose metabolism in young men with LBW. In addition, we found that the young, healthy men with LBW exhibited hepatic insulin resistance. However, the study does not support the hypothesis that muscle mitochondrial dysfunction per se is the underlying key metabolic defect that explains or precedes whole body insulin resistance in LBW subjects at risk for developing type 2 diabetes.

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