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      Relationship between peripheral arterial disease severity determined by the Glass classification and triglyceride-glucose index; novel association and novel classification system Translated title: Relación entre la gravedad de la enfermedad arterial periférica determinada por la clasificación GLASS y el índice de triglicéridos-glucosa; nueva asociación y nuevo sistema de clasificación


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          Abstract Peripheral arterial disease is a serious clinical manifestation caused by atherosclerosis. It is one common cause of morbidity and mortality worldwide. It is commonly seen in males, and its (prevelance) increases with age. It is most prevalent with smoking, hypertension, diabetes mellitus and hyperlipidemia. Novel studies investigate the relationship between triglyceride-glucose index (TyG) and cardiovascular diseases. Studies investigating the association of this index and peripheral arterial disease and disease severity are generally done by using The Trans-Atlantic Inter-Society Consensus (TASC) classification. We aimed to study this association by using the new Global Limb Anatomic Staging System (GLASS) classification. Two hundred patients between 25 to 90 years old diagnosed with peripheral arterial disease and admitted to the hospital for peripheral arterial angiography between July 2021 and December 2021, were evaluated retrospectively with blood parameters and angiographic images. Patients were divided into two groups: moderate (group 1; n=58) and severe (group 2; n=142) according to the GLASS classification. No statistical differences were observed for comorbidities and repeated interventional procedure rates (p=0.164). Triglyceride values were found to be statistically different between groups (p=0.040). TyG was found higher in group 2 (p= 0.04). According to the binary logistic regression model, only TyG was found to have a significant effect as a diagnostic factor (p=0.011). TyG was also significantly correlated with the Rutherford (p=0.012) and GLASS classification severity (p<0.001). Peripheral arterial disease and disease severity could be easily monitored with simple calculable TyG. In this way, precautions could be taken, and morbidities could be prevented.

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          Resumen La enfermedad arterial periférica es una manifestación clínica importante causada por la aterosclerosis. Es una causa común de morbilidad y mortalidad en todo el mundo. Se ve comúnmente en hombres y la prevalencia aumenta con la edad. Es más común con el tabaquismo, la hipertensión, la diabetes mellitus y la hiperlipidemia. Nuevos estudios investigan la relación entre el índice de triglicéridos-glucosa (TyG) y las enfermedades cardiovasculares. Los estudios que investigan la asociación de este índice y la enfermedad arterial periférica generalmente se realizan utilizando la clasificación de TASC. Nuestro objetivo fue estudiar esta asociación utilizando la nueva clasificación de GLASS (sistema global de estadificación anatómica de extremidades). Doscientos pacientes entre 25 a 90 años con diagnóstico de enfermedad arterial periférica e ingresados al hospital para angiografía arterial periférica entre julio de 2021 y diciembre de 2021, fueron evaluados retrospectivamente con parámetros sanguíneos e imágenes angiográficas. Los pacientes se dividieron en dos grupos: leves (grupo 1; n=58) y graves (grupo 2; n=142) según la clasificación de GLASS. No se observaron diferencias estadísticas para las comorbilidades y las tasas de procedimientos intervencionistas repetidos (p = 0,164). Los valores de triglicéridos se encontraron significativamente diferentes entre los grupos (p= 0,04). El índice de triglicéridos-glucosa se encontró más alto en el grupo 2 (p= 0,04). Según el modelo de regresión logística binaria, solo el índice de triglicéridos-glucosa resultó tener un efecto significativo como factor diagnóstico (p=0,011). El índice de triglicéridos-glucosa también se correlacionó significativamente con la gravedad de la clasificación de Rutherford (p=0,012) y la clasificación de GLASS (p<0,001). La enfermedad arterial periférica y la gravedad de la enfermedad podrían controlarse fácilmente con TyG calculable simple. De esta manera, se podrían tomar precauciones y prevenir morbilidades.

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          Mechanisms of Insulin Action and Insulin Resistance

          The 1921 discovery of insulin was a Big Bang from which a vast and expanding universe of research into insulin action and resistance has issued. In the intervening century, some discoveries have matured, coalescing into solid and fertile ground for clinical application; others remain incompletely investigated and scientifically controversial. Here, we attempt to synthesize this work to guide further mechanistic investigation and to inform the development of novel therapies for type 2 diabetes (T2D). The rational development of such therapies necessitates detailed knowledge of one of the key pathophysiological processes involved in T2D: insulin resistance. Understanding insulin resistance, in turn, requires knowledge of normal insulin action. In this review, both the physiology of insulin action and the pathophysiology of insulin resistance are described, focusing on three key insulin target tissues: skeletal muscle, liver, and white adipose tissue. We aim to develop an integrated physiological perspective, placing the intricate signaling effectors that carry out the cell-autonomous response to insulin in the context of the tissue-specific functions that generate the coordinated organismal response. First, in section II, the effectors and effects of direct, cell-autonomous insulin action in muscle, liver, and white adipose tissue are reviewed, beginning at the insulin receptor and working downstream. Section III considers the critical and underappreciated role of tissue crosstalk in whole body insulin action, especially the essential interaction between adipose lipolysis and hepatic gluconeogenesis. The pathophysiology of insulin resistance is then described in section IV. Special attention is given to which signaling pathways and functions become insulin resistant in the setting of chronic overnutrition, and an alternative explanation for the phenomenon of ‟selective hepatic insulin resistanceˮ is presented. Sections V, VI, and VII critically examine the evidence for and against several putative mediators of insulin resistance. Section V reviews work linking the bioactive lipids diacylglycerol, ceramide, and acylcarnitine to insulin resistance; section VI considers the impact of nutrient stresses in the endoplasmic reticulum and mitochondria on insulin resistance; and section VII discusses non-cell autonomous factors proposed to induce insulin resistance, including inflammatory mediators, branched-chain amino acids, adipokines, and hepatokines. Finally, in section VIII, we propose an integrated model of insulin resistance that links these mediators to final common pathways of metabolite-driven gluconeogenesis and ectopic lipid accumulation.
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            Association between insulin resistance and the development of cardiovascular disease

            For many years, cardiovascular disease (CVD) has been the leading cause of death around the world. Often associated with CVD are comorbidities such as obesity, abnormal lipid profiles and insulin resistance. Insulin is a key hormone that functions as a regulator of cellular metabolism in many tissues in the human body. Insulin resistance is defined as a decrease in tissue response to insulin stimulation thus insulin resistance is characterized by defects in uptake and oxidation of glucose, a decrease in glycogen synthesis, and, to a lesser extent, the ability to suppress lipid oxidation. Literature widely suggests that free fatty acids are the predominant substrate used in the adult myocardium for ATP production, however, the cardiac metabolic network is highly flexible and can use other substrates, such as glucose, lactate or amino acids. During insulin resistance, several metabolic alterations induce the development of cardiovascular disease. For instance, insulin resistance can induce an imbalance in glucose metabolism that generates chronic hyperglycemia, which in turn triggers oxidative stress and causes an inflammatory response that leads to cell damage. Insulin resistance can also alter systemic lipid metabolism which then leads to the development of dyslipidemia and the well-known lipid triad: (1) high levels of plasma triglycerides, (2) low levels of high-density lipoprotein, and (3) the appearance of small dense low-density lipoproteins. This triad, along with endothelial dysfunction, which can also be induced by aberrant insulin signaling, contribute to atherosclerotic plaque formation. Regarding the systemic consequences associated with insulin resistance and the metabolic cardiac alterations, it can be concluded that insulin resistance in the myocardium generates damage by at least three different mechanisms: (1) signal transduction alteration, (2) impaired regulation of substrate metabolism, and (3) altered delivery of substrates to the myocardium. The aim of this review is to discuss the mechanisms associated with insulin resistance and the development of CVD. New therapies focused on decreasing insulin resistance may contribute to a decrease in both CVD and atherosclerotic plaque generation.
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              Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II).


                Author and article information

                Investigación Clínica
                Invest. clín
                Instituto de Investigaciones Clínicas "Dr. Américo Negrette", Facultad de Medicina, Universidad del Zulia (Maracaibo, Zulia, Venezuela )
                December 2022
                : 63
                : 4
                : 363-375
                [1] Isparta orgnameIsparta City Hospital orgdiv1Cardiovascular Surgery Department Turkey
                S0535-51332022000400363 S0535-5133(22)06300400363

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.

                : 20 July 2022
                : 14 March 2022
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 48, Pages: 13

                SciELO Venezuela

                peripheral arterial disease,insulin resistance,triglyceride-glucose index,GLASS classification,resistencia a la insulina,indice de triglicéridos-glucosa,clasificación de GLASS,enfermedad arterial periférica


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