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Features of Lipid Metabolism in Diabetes Mellitus and Ischemic Heart Disease
Published in E.I. Sokolov, Obesity and Diabetes Mellitus, 2020
The deep studying of the risk factors of IHD by clinicians, morphologists, and biochemists during recent years brought to light one of the important disorders of metabolism in the pathogenesis of atherosclerosis, namely, syndrome X — a combination of hyperinsulinemia and insulin resistance. Syndrome X is a pathogenetically integrated disorder of metabolism including hyperinsulinemia, DM, and obesity, on the one hand, and disturbance of the tolerance to glucose and hypertension on the other. Degradation of the hormonal-mediator units of metabolism in syndrome X leads to disorder of the physiological regulator mechanisms and to the progressing of IHD.
Obesity
Published in Geoffrey P. Webb, Nutrition, 2019
This myriad of metabolic consequences of insulin resistance is termed the metabolic syndrome or sometimes “syndrome X”. Whilst people with this syndrome are not aware of the acute symptoms of diabetes, their condition does nevertheless predispose them to cardiovascular disease in just the same way as those suffering from overt type-2 diabetes. Many people with syndrome X will go on to develop overt type-2 diabetes. Any individual who meets three of the following criteria would be classified as syndrome X: High waist circumference Moderate fasting hyperglycaemia or raised glycosylated haemoglobin Elevated blood pressure Elevated blood triacylglycerol levels Low plasma HDL levels.
A Protein-Centric Perspective for Skeletal Muscle Metabolism and Cardiometabolic Health
Published in Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss, Nutrition and Cardiometabolic Health, 2017
Donald K. Layman, Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss
Cardiometabolic disorders express a cluster of metabolic and physiological risk factors including elevated body fat, abnormal blood triglycerides, and insulin resistance (Grundy et al., 2004). This cluster of factors was originally termed “syndrome X” or the “metabolic syndrome.” Subsequent research questioned if the metabolic syndrome was fundamentally a lipid disorder, dysfunction of glycemic regulations, a consequence of obesity, or declining function of skeletal muscle (Reaven, 1996). These questions led to nutrition studies testing an array of diet combinations with higher or lower amounts of fat, carbohydrates, and protein. Diets that reduce energy intake with higher protein and lower carbohydrates have been shown to be beneficial for cardiometabolic health (Layman et al., 2008). These diets produce a greater loss of body weight and body fat while minimizing the loss of lean tissues and lead to improvements in glycemic regulations and dyslipidemia (Krieger et al., 2006; Wycherley et al., 2012). In total, higher-protein diets appear to reverse many of the risk factors associated with the metabolic syndrome. While the outcomes of these diets appear beneficial, defining the specific role of protein is often confounded by changes in total energy and carbohydrates.
Gut microbiota associations with metabolic syndrome and relevance of its study in pediatric subjects
Published in Gut Microbes, 2021
Ana K. Carrizales-Sánchez, Tomás García-Cayuela, Carmen Hernández-Brenes, Carolina Senés-Guerrero
MetS, also known as “Syndrome X”, is an acquired condition characterized by possessing at least three of the following cardio-metabolic abnormalities: high blood pressure, increased central adiposity, hyperglycemia, high triglyceride levels, and decreased high-density lipoprotein cholesterol (HDL-c) levels.7 Its pathophysiology is a result of genetic predisposition, demographic background, and lifestyle factors such as sedentarism and diets rich in refined carbohydrates, sugars and fats.8,9 Notably, a relationship between gut microbiota and MetS was published a decade ago, where 16S rRNA sequencing determined that Toll-like receptor (TLR) 5 knock-out mice (T5KO) had gut microbial alterations linked with increased low-grade proinflammatory signaling that ended in MetS, validating it with gut microbiota transplantation from T5KO into wild-type (WT) germ-free mice, where all of the key features of MetS were developed after the procedure.2
Family history of diabetes mellitus and long-term endocrine morbidity of the offspring
Published in Gynecological Endocrinology, 2020
Yuval Alon, Tamar Wainstock, Eyal Sheiner, Gali Pariente
It is important that the medical provider be aware of the patient’s family history, as this information could reflect potential metabolic and cardiovascular disorders from which the patient might suffer in the future [11–15]. For example, the effect of maternal malnutrition during pregnancy on the health status of the offspring is known as ‘Syndrome X’ [16]. There are several different hypotheses and pathways suggested in order to account for the phenomenon of Syndrome X. According to Barker et al., the conditions in the intra-uterine environment of pregnant mothers lead to malnutrition in early fetal life, causing cellular changes in the fetus that result in long-term endocrine implications, including Type 2 DM, hypertension and organ malfunction [16]. However, in a previous study conducted by our group, we found that maternal family history of DM (FHDM) resulted in macrosomia and higher rates of cesarean delivery. These results were reflected even when investigating the role of a FHDM while controlling for DM and GDM in the mother, suggesting a long-term effect that is not necessarily related to the intra-uterine environment [17]. These results led us to believe that if a long-term effect exists in the mother, it should also have an impact later on in the offspring life. Accordingly, the aim of the present study was to determine whether being born to a mother without diabetes, yet with a FHDM, increases the risk for long-term endocrine morbidity of the offspring.
NASH (nonalcoholic steatohepatitis), diabetes, and macrovascular disease: multiple chronic conditions and a potential treatment at the metabolic root
Published in Expert Opinion on Investigational Drugs, 2020
The concept of Syndrome X, also known as metabolic syndrome or insulin resistance syndrome, was introduced by Reaven in 1988 [13]. Reaven and his colleagues proposed that resistance, or reduced responsiveness of tissues to insulin action, and the resulting hyperinsulinemia were ‘involved in the etiology of and clinical course of three related diseases – NIDDM, hypertension, and CAD (coronary artery disease).’ Subsequently, fatty liver disease has also been added to this list. The concept holds that a metabolic disturbance turns down the cellular responses to insulin and in turn the pancreatic beta cells are stimulated to secrete more insulin. The downstream changes in metabolism in response to the combination of higher insulin and reduced response to insulin adversely affect cardiovascular function. This insulin resistance also continues the drive on the pancreatic beta cells to produce more and more insulin. In some individuals, this results in progressive impairment of pancreatic beta cell function and, in turn, progressive increases in plasma glucose. When pancreatic compensation fails, plasma glucose levels continue to rise and may eventually reach consensus clinical criteria termed as type 2 diabetes.