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Impaired Fasting Glucose Pathophysiology

Dr. Rose's Peripheral Brain--diabetes--definitions, Classification, Pathophysiology

Dr. Rose's Peripheral Brain--diabetes--definitions, Classification, Pathophysiology

DIABETES--DEFINITIONS, CLASSIFICATION,PATHOPHYSIOLOGY "A group of metabolic disorders characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both" Diagnostic Criteria--Must meet one of the criteria below on two separate days (doesn't have to be the same criterion both times) Sx of DM (polyuria, polydipsia, unexplained weight loss) plus random blood glucose > 200 Fasting (>8h) glucose > 125mg/dl (probably as accurate as, and more reproducible than, the 2h post-glucose reading in the oral glucose tolerance test) 2h glucose > 200 mg/dl at any of the draws done during an oral glucose tolerance test (75g glucose after an overnight fast, check glucose at 1,2, and 3h) Note that plasma glucose values are us. 10-15% higher than whole blood glucose values HbA1c can be used to diagnose DM (if 6.5% or greater and confirmed with a repeat), per an "International Expert Committee" including representatives of the ADA (Diab. Care 32:1327, 2009-JW) II. Classification and Pathophysiology--"For theclinician and patient it is less important to label theparticular type of diabetes than it is to understand thepathogenesis of the hyperglycemia and to treat iteffectively" Type 1 diabetes--due to absolute deficiency in insulin secretion prine to DKA. Usually starts in childhood or adolescence but can occur at any age Immune-Mediated (autoimmune destruction of pancreatic beta-cells) Serologic evidence present in 85-90% of pts with type 1 DM (anti-ICA, IAA, GAD, IA-2, etc.) Serologic evidence suggests an association between infection with enterovirus and onset of type 1 diabetes. (BMJ 342:d35, 2011-JW) Idiopathic (no evidence for immune-mediated beta-cell destruction) Type 2 diabetes--due to insulin resistance and relative deficiency in insulin secretion; Continue reading >>

Classification, Pathophysiology, Diagnosis And Management Of Diabetes Mellitus

Classification, Pathophysiology, Diagnosis And Management Of Diabetes Mellitus

University of Gondar, Ethopia *Corresponding Author: Habtamu Wondifraw Baynes Lecturer Clinical Chemistry University of Gondar, Gondar Amhara 196, Ethiopia Tel: +251910818289 E-mail: [email protected] Citation: Baynes HW (2015) Classification, Pathophysiology, Diagnosis and Management of Diabetes Mellitus. J Diabetes Metab 6:541. doi:10.4172/2155-6156.1000541 Copyright: © 2015 Baynes HW. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Diabetes & Metabolism Abstract Diabetes Mellitus (DM) is a metabolic disorder characterized by the presence of chronic hyperglycemia either immune-mediated (Type 1 diabetes), insulin resistance (Type 2), gestational or others (environment, genetic defects, infections, and certain drugs). According to International Diabetes Federation Report of 2011 an estimated 366 million people had DM, by 2030 this number is estimated to almost around 552 million. There are different approaches to diagnose diabetes among individuals, The 1997 ADA recommendations for diagnosis of DM focus on fasting Plasma Glucose (FPG), while WHO focuses on Oral Glucose Tolerance Test (OGTT). This is importance for regular follow-up of diabetic patients with the health care provider is of great significance in averting any long term complications. Keywords Diabetes mellitus; Epidemiology; Diagnosis; Glycemic management Abbreviations DM: Diabetes Mellitus; FPG: Fasting Plasma Glucose; GAD: Glutamic Acid Decarboxylase; GDM: Gestational Diabetes Mellitus; HDL-cholesterol: High Density Lipoprotein cholesterol; HLA: Human Leucoid Antigen; IDD Continue reading >>

What Is Prediabetes? Learn More About Causes & Symptoms Of Prediabetes

What Is Prediabetes? Learn More About Causes & Symptoms Of Prediabetes

Prediabetes is a condition defined by the presence of impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) that has not yet reached the threshold for type 2 diabetes mellitus (T2D); the metabolic syndrome is also considered a prediabetes equivalent (1,2). Prediabetes raises short-term absolute risk of T2D by 3- to 10-fold (2). In the United States, 86 million people, or 37% of the US population, have prediabetes, and it is estimated that up to 70% of people with prediabetes may develop T2D during their lifetimes (3,4). According to a National Health and Nutrition Examination Survey (NHANES) conducted in 2010, while one-third of US residents have prediabetes, only 11% have received a formal diagnosis from a physician (5). In a 2006 NHANES study, no patients reported receiving oral antihyperglycemic agents, while the percentage who received a physician recommendation for exercise or diet was 31.7% and 33.4%, respectively. Furthermore, among those diagnosed with prediabetes, 68% had tried to lose or control their weight, 60% had reduced dietary fat or calories, 55% had increased their physical activity or exercise, and 42% had engaged in all 3 activities (6). Prediabetes is a state of abnormal glucose homeostasis characterized by the presence of IFG, IGT, or both. This abnormal glucose homeostasis is a result of both beta-cell failure and insulin resistance (2,7-9). Prediabetes and subsequent T2D likely develop as a result of polygenic defects that predispose affected individuals to the disease. Environmental factors such as a sedentary lifestyle and a high-fat diet can exacerbate defects in both insulin secretion from pancreatic beta-cells and insulin action in muscle and adipose tissues. The modest hyperglycemia characteristic of the prediabetic state Continue reading >>

Effects And Mechanism Of Moderate Aerobic Exercise On Impaired Fasting Glucose Improvement

Effects And Mechanism Of Moderate Aerobic Exercise On Impaired Fasting Glucose Improvement

Exercise is beneficial for blood glucose metabolism. However, whether moderate aerobic exercise could improve impaired fasting glucose is unknown. And the mechanism is also needed to investigate. A cross-sectional research was performed and 120 participants with impaired fasting glucose (IFG) were randomly assigned into active and controlled groups. Briefly, participants in active group were required to take moderate aerobic exercise at least 30min for five times per week, whereas in controlled group, participants were also advised to take exercise but not mandatorily required the same degree as that of active group. At baseline and 3months follow-up, laboratory and demographic variables were compared. At baseline, no significant between-group differences were observed. Generally, leukocyte ROCK2 activity in the active and controlled groups were 58.7 6.0mg/mL and 60.2 7.3mg/mL, and daily average exercise time at baseline in both groups was extremely little, with 5.2 3.8min and 5.9 3.5min, respectively. After 3months follow-up, 52 and 56 participants in the active and controlled groups completed the whole program. Compared to baseline, leukocyte ROCK2 activity and daily average exercise time were improved in both groups. Nonetheless, compared to the controlled group, leukocyte ROCK2 activity was reduced more profoundly and the daily average exercise time was longer in the active group (37.5 6.3min versus 18.3 7.2min, p < 0.05). Moreover, the percentage of IFG in the active group was decreased more prominently than the controlled group (76.9% versus 82.1%, p < 0.05). Multivariate regression analyses revealed that exercise time and leukocyte ROCK2 activity was significantly associated with IFG, with OR of 0.836 (active group versus controlled group, 95% CI 0.825-0.852, p Continue reading >>

Glucose Intolerance: Practice Essentials, Pathophysiology, Etiology

Glucose Intolerance: Practice Essentials, Pathophysiology, Etiology

Author: Samuel T Olatunbosun, MD, FACP, FACE; Chief Editor: George T Griffing, MD more... Glucose intolerance is an umbrella term for a group of metabolic conditionsthat result in higher than normal blood glucose levels. Both theWorld Health Organization (WHO) and the American Diabetes Association (ADA) have released classification systems and diagnostic criteria fordiabetes mellitus (DM) and allied categories of glucose intolerance. [ 1 , 2 , 3 ] Although similiar, there are a number of variances in recommendations which may result in differences in an individuals classification. The major categories of the disorders of glycemia or glucose tolerance are as follows: Type 1 diabetes mellitus (DM)(due to autoimmune B-cell destruction, usually leading to absolute insulin deficiency) Type 2 diabetes mellitus(due to a progressive loss of B-cell insulin secretion frequently on the background of insulin resistance) Gestational diabetes mellitus (GDM) (diabetes diagnosed in the second or third trimester of pregnancy that was not clearly overt diabetes prior to gestation) [ 4 ] Specific types of diabetes due to other causes (such as neonatal diabetes and maturity-onset diabetes of the young, diseases of the exocrine pancreas, and drug- or chemical-induced diabetes) Impaired glucose tolerance (prediabetes/intermediate hyperglycemia) Impaired fasting glucose (prediabetes/intermediate hyperglycemia) Conditions secondarily associated with glucose intolerance also occur. Etiologic types and stages of the major disorders of glucose intolerance are shown in the image below. Etiologic types and stages of the major disorders of glucose tolerance. In most cases, the diagnosis of a type of diabetes or glucose intolerance is based on the patients condition at the time, but not all patients Continue reading >>

Pathophysiology And Aetiology Of Impaired Fasting Glycaemia And Impaired Glucose Tolerance: Does It Matter For Prevention And Treatment Of Type 2 Diabetes?

Pathophysiology And Aetiology Of Impaired Fasting Glycaemia And Impaired Glucose Tolerance: Does It Matter For Prevention And Treatment Of Type 2 Diabetes?

1. Diabetologia. 2009 Sep;52(9):1714-23. doi: 10.1007/s00125-009-1443-3. Epub 2009Jul 10. Pathophysiology and aetiology of impaired fasting glycaemia and impaired glucose tolerance: does it matter for prevention and treatment of type 2 diabetes? Faerch K(1), Borch-Johnsen K, Holst JJ, Vaag A. (1)Steno Diabetes Center, Niels Steensens Vej 2, 2820, Gentofte, Denmark. [email protected] Prior to the development of type 2 diabetes, glucose levels increase into theprediabetic states of isolated impaired fasting glycaemia (i-IFG), isolatedimpaired glucose tolerance (i-IGT), or combined IFG/IGT. A better understandingof the aetiology and pathophysiology of the prediabetic states might give a basisfor the development of individualised prevention and treatment strategies fortype 2 diabetes. Several studies have examined mechanisms and potentialaetiological factors leading to the development of the different prediabeticstates. The pathophysiology of i-IFG seems to include the following key defects: reduced hepatic insulin sensitivity, stationary beta cell dysfunction and/orchronic low beta cell mass, altered glucagon-like peptide-1 secretion andinappropriately elevated glucagon secretion. Conversely, the prediabetic statei-IGT is characterised by reduced peripheral insulin sensitivity, near-normalhepatic insulin sensitivity, progressive loss of beta cell function, reducedsecretion of glucose-dependent insulinotropic polypeptide and inappropriatelyelevated glucagon secretion. Individuals developing combined IFG/IGT exhibitsevere defects in both peripheral and hepatic insulin sensitivity as well as aprogressive loss of beta cell function. The aetiologies of i-IFG and i-IGT alsoseem to differ, with i-IFG being predominantly related to genetic factors,smoking and male sex, while i-IGT is Continue reading >>

Prediabetes In Patients With Stroke Or Transient Ischemic Attack: Prevalence, Risk And Clinical Management

Prediabetes In Patients With Stroke Or Transient Ischemic Attack: Prevalence, Risk And Clinical Management

Abstract Background: The prevalence of diabetes is emerging worldwide and is an important modifiable risk factor for stroke. People with prediabetes, an intermediate metabolic state between normal glucose metabolism and diabetes, have a tenfold increased risk of developing diabetes compared to those with a normal glucose metabolism. Prediabetes is comprised of impaired fasting glucose and/or impaired glucose tolerance and/or disturbed glycosylated hemoglobin levels. Prediabetes is highly prevalent in nondiabetic patients with transient ischemic attack (TIA) or ischemic stroke and nearly doubles their risk of stroke. This offers new options for secondary stroke prevention. Summary: Several detection methods exist for identifying (pre)diabetes, including fasting plasma glucose, 2-hour postload glucose and glycosylated hemoglobin levels. The concordance between these tests is not 100%, and they seem to be complementary. Screening for (pre)diabetes after stroke with fasting plasma glucose levels alone is insufficient, and 2-hour postload glucose and/or glycosylated hemoglobin levels should be determined as well. The prevalence of prediabetes in previously nondiabetic patients with a recent TIA or stroke ranges from 23 to 53%. This high prevalence in the acute phase after stroke can be transient or persistent, representing undiagnosed abnormal glucose metabolism. Impaired fasting glucose and impaired glucose tolerance have different pathophysiological mechanisms, including hepatic insulin resistance and muscle insulin resistance, respectively. Prediabetes seems to be a modest predictor for stroke, but doubles the risk for recurrent stroke. The relation between prediabetes after stroke and functional outcome is still unknown. However, it is most likely that prediabetes is a r Continue reading >>

Impaired Fasting Glycemia

Impaired Fasting Glycemia

A person with impaired fasting glycemia isn't able to process glucose as efficiently as they should be able to Impaired fasting glycemia (IFG) may also be known as pre-diabetes or metabolic syndrome. Impaired fasting glycemia occurs when blood glucose levels in the body are elevated during periods of fasting , but not enough to prompt a diagnosis of diabetes. Effectively, a person with impaired fasting glycemia isnt able to process glucose as efficiently as they should be able to. What are the health implications of impaired fasting glycemia? People with impaired fasting glycemia face a greater risk of developing type 2 diabetes, despite having less of a risk than those with impaired glucose tolerance. The risk of developing cardiovascular disease is also lower than for people with impaired glucose tolerance . What does impaired fasting glycemia mean? Impaired fasting glycemia (IFG) means that the body cannot regulate glucose as efficiently as it should be able to. Glucose is usually carried around the body where it is absorbed and made into energy. Insulin regulates the concentration of glucose in the blood. IFG occurs when this process isnt functioning as effectively as it could, and effects millions of people in the UK. What are the symptoms of impaired fasting glycemia? Unfortunately, IFG may exhibit very little in the way of symptoms, meaning diagnosis often takes a long time. Many people diagnosed with IFG are overweight, have high blood pressure, increased cholesterol levels or a family history of IFG. So how do I know if my IFG becomes type 2 diabetes? IFG increases type 2 diabetes risk, so go straight to your doctor or healthcare professional if you feel unnaturally thirsty, pass more urine than usual, have recurrent infections, have blurred vision, or if your Continue reading >>

Impaired Fasting Glucose

Impaired Fasting Glucose

Impaired fasting glucose, or Impaired Fasting Glycemia (IFG) is a type of prediabetes, in which a person's blood sugar levels during fasting are consistently above the normal range, but below the diagnostic cut-off for a formal diagnosis of diabetes mellitus.[1] Together with impaired glucose tolerance, it is a sign of insulin resistance. In this manner, it is also one of the conditions associated with Metabolic Syndrome. Those with impaired fasting glucose are at an increased risk of vascular complications of diabetes, though to a lesser extent. The risks are cumulative, with both higher blood glucose levels, and the total amount of time it spends elevated, increasing the overall complication rate. IFG can eventually progress to type 2 diabetes mellitus without intervention, which typically involves lifestyle modification. Those with impaired fasting glucose have a 1.5 fold increased risk of developing clinical diabetes within 10 years, when compared to the general population. Some studies suggest that without lifestyle changes, IFG will progress to clinically diagnosable diabetes in just under 3 years, on average.[2] Impaired fasting glucose is often, though not always, associated with impaired glucose tolerance, though it may occur in isolation, with such persons having a normal response to a glucose tolerance test. Signs and Symptoms[edit] Impaired fasting glucose is often without any signs or symptoms, other than higher than normal glucose levels being detected in an individual's fasting blood sample. There may be signs and symptoms associated with elevated blood glucose, though these are likely to be minor, with significant symptoms suggestive of complete progression to type 2 diabetes. Such symptoms include:[3] Increased thirst Increased urination, especially wak Continue reading >>

Prediabetes: A Position Statement From The Australian Diabetes Society And Australian Diabetes Educators Association

Prediabetes: A Position Statement From The Australian Diabetes Society And Australian Diabetes Educators Association

Summary Prediabetes, the presence of impaired fasting glucose/glycaemia and/or impaired glucose tolerance, affects about 16.4% of Australian adults. People with prediabetes are at increased risk of developing diabetes, and cardiovascular and other macrovascular disease. Management includes reducing cardiovascular disease risk factors, specifically lipid and blood pressure abnormalities, and smoking-cessation counselling. To help prevent progression to diabetes, people with prediabetes who are overweight or obese require intensive lifestyle intervention. Medication to help prevent diabetes may also be used, but only after a minimum of 6 months of lifestyle intervention. In people with prediabetes, there is no role for routinely testing: capillary blood glucose; glycated haemoglobin (HbA1c) levels; serum insulin or pancreatic C-peptide levels; or testing for ischaemic heart disease or the microvascular complications of diabetes. Follow-up assessment of glycaemia in prediabetes requires a formal 75 g oral glucose tolerance test, initially performed annually, with subsequent individualised testing frequency. Continue reading >>

Impaired Glucose Tolerance And Impaired Fasting Glucose

Impaired Glucose Tolerance And Impaired Fasting Glucose

Impaired glucose tolerance and impaired fasting glucose form an intermediate stage in the natural history of diabetes mellitus. From 10 to 15 percent of adults in the United States have one of these conditions. Impaired glucose tolerance is defined as two-hour glucose levels of 140 to 199 mg per dL (7.8 to 11.0 mmol) on the 75-g oral glucose tolerance test, and impaired fasting glucose is defined as glucose levels of 100 to 125 mg per dL (5.6 to 6.9 mmol per L) in fasting patients. These glucose levels are above normal but below the level that is diagnostic for diabetes. Patients with impaired glucose tolerance or impaired fasting glucose have a significant risk of developing diabetes and thus are an important target group for primary prevention. Risk factors for diabetes include family history of diabetes, body mass index greater than 25 kg per m2, sedentary lifestyle, hypertension, dyslipidemia, history of gestational diabetes or large-for-gestational-age infant, and polycystic ovary syndrome. Blacks, Latin Americans, Native Americans, and Asian-Pacific Islanders also are at increased risk for diabetes. Patients at higher risk should be screened with a fasting plasma glucose level. When the diagnosis of impaired glucose tolerance or impaired fasting glucose is made, physicians should counsel patients to lose 5 to 7 percent of their body weight and engage in moderate physical activity for at least 150 minutes per week. Drug therapy with metformin or acarbose has been shown to delay or prevent the onset of diabetes. However, medications are not as effective as lifestyle changes, and it is not known if treatment with these drugs is cost effective in the management of impaired glucose tolerance. Definitions and Epidemiology An expert committee sponsored by the American Di Continue reading >>

Insulin Secretory Defect And Insulin Resistance In Isolated Impaired Fasting Glucose And Isolated Impaired Glucose Tolerance

Insulin Secretory Defect And Insulin Resistance In Isolated Impaired Fasting Glucose And Isolated Impaired Glucose Tolerance

Insulin Secretory Defect and Insulin Resistance in Isolated Impaired Fasting Glucose and Isolated Impaired Glucose Tolerance 1Division of Clinical Nutrition and Internal Medicine, Okayama Prefectural University, Okayama 719-1197, Japan 2Preemptive Medicine and Lifestyle-Related Disease Research Center, Kyoto University Hospital, Kyoto 606-8507, Japan 3Faculty of Computer Science and Systems Engineering, Okayama Prefectural University, Okayama 719-1197, Japan 4Division of Diabetes and Endocrinology, Kyoto Preventive Medical Center, Kyoto 604-8491, Japan 5Kyoto Institute of Health Science, Kyoto 604-0845, Japan 6Center for Preventive Medicine, St. Lukes International Hospital, Tokyo 104-6591, Japan 7Faculty of Health and Welfare Science, Okayama Prefectural University, Okayama 719-1197, Japan 8Center for Diabetes, Endocrinology and Metabolism, Kansai Electric Power Hospital, Osaka 553-0003, Japan 9Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kobe 650-0047, Japan 10Department of Diabetes and Endocrinology, Saiseikai Noe Hospital, Osaka 536-0001, Japan 11Department of Diabetes and Clinical Nutrition, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan Received 21 June 2015; Accepted 18 August 2015 Copyright 2016 Sae Aoyama-Sasabe et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Objective. To investigate the characteristics of isolated impaired glucose tolerance (IGT) and isolated impaired fasting glucose (IFG), we analyzed the factors responsible for elevation of 2-hour postchallenge plasma glucose (2 h PG) and fasting plasm Continue reading >>

Pathophysiology Of Diabetes Mellitus Type 2: Beyond The Duo Insuli...

Pathophysiology Of Diabetes Mellitus Type 2: Beyond The Duo Insuli...

Hospital de Clnicas. Caracas. Venezuela. Dept. of Surgery. University of Mlaga. Mlaga. Spain. T2DM involves at least two primary pathogenic mech- anisms: (a) a progressive decline in pancreatic islet cell function resulting in reduced insulin secretion and (b) peripheral insulin resistance resulting in a decrease in the metabolic responses to insulin. This dynamic interaction between insulin secretion and insulin resistance is essen- tial to the maintenance of normal glucose tolerance (NGT). The transition from the normal control of glucose metabolism to type 2 diabetes mellitus occurs through the intermediate states of altered metabolism that worsen over time. The first state of the disease is known as predi- abetes, and consists of a set of metabolic disorder charac- terized by a great hyperglycemia, enough to increase of retinopathies, nephropathies and neuropathies incidence. If we advance in the T2DM temporal sequence we found a remarkable change in the pancreatic lation that form the Langerhans islets, mainly caused by amylin fibers accumulation over these cells from polypeptide hormone called amyloid polypeptide or IAPP. The IAPP hypersecretion and amylin fibers depo- sition attached to the endoplasmic reticulum stress caused by excessive workload due to biosynthesis over- In addition to these alterations, we must also consider the changes observed in incretins profiles like GIP (glucose- dependent insulinotropic polypeptide) and GLP-1 (glucagon-like peptide 1) directly related to glucose homeostasis maintenance. Risk factors that predispose to a healthy individual to develop T2DM are several, but the most important is the obesity. The body mass index (BMI) has been used in numerous epidemiological studies as a powerful indicator of T2DM risk. Lipotoxicity cause Continue reading >>

Pathogenesis Of Prediabetes: Role Of The Liver In Isolated Fasting Hyperglycemia And Combined Fasting And Postprandial Hyperglycemia

Pathogenesis Of Prediabetes: Role Of The Liver In Isolated Fasting Hyperglycemia And Combined Fasting And Postprandial Hyperglycemia

Glucose production, gluconeogenesis, glycogenolysis, and glucose disappearance were measured before and during a hyperinsulinemic clamp using [6,6-2H2]glucose and the deuterated water method corrected for transaldolase exchange. Fasting glucose production was higher (P < .0001) in subjects with IFG/NGT than in those with NFG/NGT because of increased rates of gluconeogenesis (P = .003). On the other hand, insulin-induced suppression of glucose production, gluconeogenesis, glycogenolysis, and stimulation of glucose disappearance all were normal. Although fasting glucose production also was increased (P = .0002) in subjects with IFG/IGT, insulin-induced suppression of glucose production, gluconeogenesis, and glycogenolysis and stimulation of glucose disappearance were impaired (P = .005). Fasting hyperglycemia is due to excessive glucose production in people with either IFG/NGT or IFG/IGT. Both insulin action and postprandial glucose concentrations are normal in IFG/NGT but abnormal in IFG/IGT. This finding suggests that hepatic and extrahepatic insulin resistance causes or exacerbates postprandial glucose intolerance in IFG/IGT. Elevated gluconeogenesis in the fasting state in IFG/NGT and impaired insulin-induced suppression of both gluconeogenesis and glycogenolysis in IFG/IGT suggest that alteration in the regulation of these pathways occurs early in the evolution of type 2 diabetes. Our objective was to examine the adiponectin axis in type 1 diabetes (T1D). T1D is an autoimmune inflammatory disease resulting from pancreatic β-cell destruction, in which insulin resistance associates with progression to disease. We measured circulating adiponectin and adiponectin receptor expression on blood-immune cells from 108 matched healthy, T1D, and type 2 diabetic subjects. We te Continue reading >>

Impaired Fasting Glucose

Impaired Fasting Glucose

Barbara J. Ehrmann, in A Comprehensive Guide to Geriatric Rehabilitation (Third Edition) , 2014 An elevated fasting glucose is one of several risk factors that is known to increase an individuals risk of developing heart disease, stroke and diabetes. These risk factors, grouped together, are called the metabolic syndrome. Other characteristics include obesity, particularly abdominal fat, hyperlipidemia and hypertension. The criteria for metabolic syndrome are met by having any three of the following risk factors, as recently defined by the American Heart Association and International Diabetes Federation: (i) an elevated waist circumference (abdominal obesity); (ii) an elevated triglyceride level of 150mg/dl or greater; (iii) a reduced high-density lipoprotein (HDL good cholesterol) level of less than 40mg/dl for men and less than 50mg/dl for women; (iv) an elevated blood pressure of 130/85mmHg or higher; and (v) an elevated fasting glucose of 100mg/dl or higher (Alberti et al., 2009). Fifty-two percent of males and 54% of females in the US over the age of 60 met the criteria for metabolic syndrome for the years 20032006 (Ervin, 2009). Karen Z. Walker, Kerin ODea, in Nutritional and Therapeutic Interventions for Diabetes and Metabolic Syndrome , 2012 Individuals with impaired fasting glucose or impaired glucose tolerance are at high risk of progression to type 2 diabetes. This disease can be delayed or prevented through changes to dietary pattern and increased physical activity. Large prospective studies following high-risk individuals for a period of 2.56 years indicate that lifestyle change may reduce the incidence of type 2 diabetes by 2868%. Moreover, diabetes incidence rates continue to be depressed many years after completion of the supervised phase of a lifestyle Continue reading >>

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