A Protein-Centric Perspective for Skeletal Muscle Metabolism and Cardiometabolic Health
Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss in Nutrition and Cardiometabolic Health, 2017
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.
Polycystic ovary syndrome
David M. Luesley, Mark D. Kilby in Obstetrics & Gynaecology, 2016
Polycystic ovary syndrome is the most common endocrine disorder to affect women during their reproductive years.1 The symptoms of PCOS include menstrual cycle disturbance and features of hyperandrogenism (hirsutism, acne, alopecia), with associated fertility problems, obesity and psychological issues. There is significant heterogeneity of presentation, such that signs and symptoms manifest across a spectrum and their severity may vary. Ovarian hyperandrogenism is thought to have genetic origins with amplification in some by hyperinsulinaemia secondary to insulin resistance, which in turn may be promoted by obesity. The primary presenting complaint itself is subject to change depending on the age and needs of the patient; for example acne may be a primary concern during adolescence whereas reduced fertility may be the main concern for an older woman. PCOS may also be associated with an increased the risk of an individual developing type 2 diabetes, the metabolic syndrome and endometrial cancer.1,2 The symptoms of PCOS may have a profound impact on psychological well-being.3 Options for treatment include lifestyle advice and a range of therapies depending upon the constellation of an individual’s problems.4
Type 2 Diabetes Mellitus
Jack L. Leahy, Nathaniel G. Clark, William T. Cefalu in Medical Management of Diabetes Mellitus, 2000
Type 2 diabetes mellitus is a common metabolic disorder that is characterized by hyperglycemia without absolute insulin deficiency, and the triad of impaired glucose uptake into insulin-sensitive tissues, with skeletal muscle most affected, increased glucose production by the liver, and impaired insulin secretion. It is typically accompanied by other metabolic disorders that share defective insulin action as part of their pathogenesis (metabolic syndrome or syndrome X), such as central obesity, hypertriglyceridemia, atherosclerosis, hypertension, and hyper- androgenism in women secondary to polycystic ovaries (PCO). In the past, type 2 diabetes was often portrayed as the "mild" form of diabetes, with little prognostic significance. We now know that nothing could be farther from the truth. Diabetes has the dubious distinction of being the number 1 cause of adult blindness, kidney failure, and nontraumatic limb amputation in much of the industrialized world; type 2 diabetes makes up the majority of these statistics because of the 10:1 ratio of affected persons versus type 1 diabetes. Moreover, the worldwide incidence of type 2 diabetes and associated illnesses is skyrocketing, which has led the World Health Organization (WHO) to designate diabetes as a health crisis. A positive development is the availability of antidiabetic drugs that act at many different sites in the glucose homeostasis system. Thus, we now have the ability to use multidrug regimens that allow most patients to attain their target goal for glycemia, and the onus is on practicing physicians to be familiar with their use.
First victim, later aggressor: How the intestinal microbiota drives the pro-inflammatory effects of dietary emulsifiers?
Published in Gut Microbes, 2018
Emilie Viennois, Benoit Chassaing
The intestinal microbiota is a vast and complex community of microorganisms that includes 1014 bacteria per intestine and about 1000 different species. Among its various functions, the gut microbiota is essential to promote maturation of the intestinal immune system, help digestion and favor calorie extraction. Besides its essential beneficial roles, the gut microbiota can also turn out to be detrimental and, if not well managed, lead to the development of inflammatory diseases, such as Inflammatory Bowel Disease (IBD)1 and metabolic syndrome.2 Inflammatory bowel diseases are severe, debilitating, and lead to a significantly increased risk to develop colon cancer that affects millions of people worldwide. Metabolic syndrome is a cluster of obesity-related disorders (high blood pressure, hyperglycemia, abnormal triglyceride and cholesterol levels) that together, substantially increase the risk of developing type-2 diabetes, cardiovascular, and/or liver diseases.
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
Jerry Colca
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.
Related Knowledge Centers
- Hyperglycemia
- Hypertriglyceridemia
- Syndrome
- Type 2 Diabetes
- Cardiovascular Disease
- Hypertension
- Insulin Resistance
- Abdominal Obesity
- High-Density Lipoprotein
- Prediabetes