Already read this title? Please accept our apologies for any inconvenience this may cause. Exclusive web offer for individuals. Pathophysiology and Management 1st Edition Emmanuel C. Add to Wish List. Toggle navigation Additional Book Information. Description Table of Contents Reviews. Summary Diabetes occurs at such an alarming rate that it is believed to be nearing epidemic proportions worldwide. Pathophysiology and Management is a comprehensive resource that examines the metabolic aberrations found in obesity that eventually lead to the development of diabetes.
By focusing on the role diet has in the cause and management of obesity and diabetes, it provides a scientific basis for the different approaches used in their treatment. The text is divided into three sections for easy reference. Section I, Pathophysiology and Treatment of Obesity, includes chapters on the neuroendocrine regulation of food intake, achieving healthy body weight through diet and exercise, and surgical and nonsurgical weight loss techniques. Section II, Pathophysiology and Treatment of Diabetes, presents discussions on Type 2 diabetes in childhood, the management of Type 2 diabetes in underrepresented minorities in the U.
Section III, The Role of Oxidative Stress in the Pathogenesis and Treatment of Diabetes and Its Complications, outlines oxidative stress in relation to Type 1 diabetes, glycemic control in Type 2 diabetes, and the vascular complications of diabetes mellitus. The text presents these topics in a comprehensive yet accessible manner, making Nutrition and Diabetes: Pathophysiology and Management an important resource for those interested in acquiring the latest information on nutrition's essential role in the cause and management of diabetes. Morgan Achieving a Healthy Body Weight: Bales and Jama L.
Opara Type 2 Diabetes in Childhood: Lien and Mark N. Fridlyand and Louis H.
Nutrition and Diabetes: Pathophysiology and Management - CRC Press Book
This group includes persons with genetic defects of beta-cell function this type of diabetes was formerly called MODY or maturity-onset diabetes in youth or with defects of insulin action; persons with diseases of the exocrine pancreas, such as pancreatitis or cystic fibrosis; persons with dysfunction associated with other endocrinopathies e. Most of the symptoms are similar in both types of diabetes but they vary in their degree and develop more rapidly in type 1 diabetes and more typical.
Some of the symptoms include weight loss, polyurea, polydipsia, polyphagia, constipation fatigue, cramps, blurred vision, and candidiasis [ 21 ]. Long lasting type 1 DM patients may susceptible to microvascular complications; [ 22 - 24 ] and macrovascular disease coronary artery, heart, and peripheral vascular diseases [ 25 ].
Most cases are diagnosed because of complications or incidentally. Carries a high risk of large vessel atherosclerosis commonly associated with hypertension, hyperlipidaemia and obesity. Most patients with type 2 diabetes die from cardiovascular complications and end stage renal disease. Geographical variation can contribute in the magnitude of the problems and to overall morbidity and mortality [ 26 - 28 ] Table 3.
Clinical characteristics of type 1 diabetes, type 2 diabetes and monogenic diabetes in children and adolescents.
Nutrition and Diabetes: Pathophysiology and Management
Adapted from Craig ME [29]. Whenever there is hyperglycemia, the brain recognizes it and send a message through nerve impulses to pancreas and other organs to decrease its effect [ 30 ]. Several features characterize type 1 diabetes mellitus as an autoimmune disease [ 32 ]:. Association of susceptibility to disease with the class II immune response genes of the major histocompatibility complex MHC; human leucocyte antigens HLA ;. Frequent occurrence of other organ specific auto- immune diseases in affected individuals or in their family members.
Most islet cell antibodies are directed against glutamic acid decarboxylase GAD within pancreatic B cells [ 33 ]. Normally, hyperglycemia leads to reduced glucagons secretion, however, in patients with T1DM, glucagons secretion is not suppressed by hyperglycemia [ 34 ]. The resultant inappropriately elevated glucagons levels exacerbate the metabolic defects due to insulin defi-ciency. Although insulin deficiency is the primary defect in T1DM, there is also a defect in the administration of insulin. Deficiency in insulin leads to uncontrolled lipolysis and elevated levels of free fatty acids in the plasma, which suppresses glucose metabolism in peripheral tissues such as skeletal muscle [ 34 ].
This impairs glucose utilization and insulin deficiency also decreases the expression of a number of genes necessary for target tissues to respond normally to insulin such as glucokinase in liver and the GLUT 4 class of glucose transporters in adipose tissue [ 34 ] explained that the major metabolic derangements, which result from insulin deficiency in T1DM are impaired glucose, lipid and protein metabolism.
Keeping in mind the intimate relationship between the secretion of insulin and the sensitivity of hormone action in the complicated control of glucose homeostasis, it is practically impossible to separate the contribution of each to the etiopathogenesis of DM2 [ 20 ]. Insulin resistance and hyperinsulinemia eventually lead to impaired glucose tolerance [ 36 ].
Except for maturity onset diabetes of the young MODY , the mode of inheritance for type 2 diabetes mellitus is unclear. MODY, inherited as an autosomal dominant trait, may result from mutations in glucokinase gene on chromosome 7p. MODY is defined as hyperglycemia diagnosed before the age of twenty-five years and treatable for over five years without insulin in cases where islet cell antibodies ICA are negative [ 26 ].
The primary events are believed to be an initial deficit in insulin secretion and in many patients relative insulin deficiency in association with peripheral insulin resistance [ 37 ]. Resistance to the action of insulin will result in impaired insulin mediated glucose uptake in the periphery by muscle and fat , incomplete suppression of hepatic glucose output and impaired triglyceride uptake by fat.
To overcome the insulin resistance, islet cells will increase the amount of insulin secreted. Endogenous glucose production is accelerated in patients with type 2 diabetes or impaired fasting glucose. Because this increase occurs in the presence of hyper insulinemia, at least in the early and intermediate disease stages, hepatic insulin resistance is the driving force of hyperglycemia of type 2 diabetes Figure 1- 7. Physiologic and Behavioral response of hyperglycemia. Adapted from Cryer [ 30 ].
Pathophysiology of Hyperglycemia and increased circulating fatty acids in type 2 Diabetes. Adapted from Pittas [ 26 ]. Panel A shows the physiological effect of a decrease in insulin coupled with a low glucose concentration in stimulating alpha-cell glucagon secretion, and Panel B shows the pathophysiological effect of beta-cell failure and the resulting loss of a decrease in insulin secretion and loss of an increase in alpha-cell glucagon secretion, despite a low glucose concentration.
Adapted from Cryer [ 39 ]. Suggested approach to screening patients at risk for diabetes. Adapted from Salomaa and Diabetes Care [ 36 , 48 ]. Schematic overview of the major areas contributing to diabetic complications. Adapted from Josephine M [ 40 ]. General management of diabetes mellitus.
Adapted from Riddle MC [ 63 ]. The identification of patients with diabetes or pre-diabetes by screening allows for earlier intervention, with potential reductions in future complication rates, although randomized trials are lacking to definitively show benefit. The patient described in the vignette has risk factors obesity, hypertension, and a family history of diabetes and should be screened Table 4 [].
As a result there are different approaches to diagnose diabetes among individuals. Adapted from ADA [42]. This test requires fasting at least eight but not more than 16 hrs. The blood is tested every 30 minutes to one hr for two or three hrs. Proteins react spontaneously in blood with glucose to form glycated derivatives. The extent of glycation of proteins is controlled by the concentration of glucose in blood and by the number of reactive amino groups present in the protein that are accessible to glucose for reaction.
All proteins with reactive sites can be glycated and the concentration of the glycated proteins that can be measured in blood is a marker for the fluctuation of blood glucose concentrations during a certain period. From a clinical diagnostic point glycated proteins with a longer life time in blood are of interest, since they reflect the exposure of these proteins to glucose for longer periods.
The life span of hemoglobin in vivo is 90 to days. During this time glycated hemoglobin A forms, being the ketoamine compound formed by combination of hemoglobin A and glucose. Several subfractions of glycated hemoglobin have been isolated. Of these, glycated hemoglobin A fraction HbA1c is of most interest serving as a retrospective indicator of the average glucose Concentration. HbA1c is recommended as an essential indicator for the monitoring of blood glucose control. Albumin is the main component of plasma proteins. As albumin also contains free amino groups, non-enzymatic reaction with glucose in plasma occurs.
Therefore glycated albumin can similarly serve as a marker to monitor blood glucose. Glycated albumin is usually taken to provide a retrospective measure of average blood glucose concentration over a period of 1 to 3 weeks. At least 6 weeks after the pregnancy ends, the woman should receive an oral glucose tolerance test and be reclassified as having diabetes, normal glucose tolerance, impaired. Women at high risk positive family history, history of GDM, marked obesity, and high risk ethnic group should be screened as soon as feasible. If the initial screening is negative, they should undergo retesting at weeks.
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The diagnosis of GDM is made if two or more of the plasma glucose values in Table 7 are met or exceeded [ 32 ]. Two or more values must be met or exceeded for a diagnosis of diabetes to be made. The test should be done in the morning after 8 to 14 hours fast. Major diagnostic criteria for diabetes and prediabetic or at-risk states. Data are adapted from the American Diabetes Association. Adapted from Salomaa and Diabetes Care [22,23]. It is unclear whether the risk of complications of diabetes differs according to whether the disease was diagnosed by means of fasting plasma glucose testing only or glycated hemoglobin testing only.
Preliminary data from a large, community- based prospective cohort study suggest that the glycated hemoglobin level, which integrates fasting and postprandial glucose levels over a longer period, might be a better predictor of certain complications especially cardiovascular disease [ 45 ]. It is also not known whether the risk of diabetes differs between patients identified as having pre-diabetes by means of glycated hemoglobin testing and those identified by means of fasting plasma glucose testing.
Such risks probably vary according to which test is used ultimately to make the diagnosis. Ongoing research is assessing the value of risk scores that incorporate not only glycemic measures but also other biomarkers and risk factors to estimate diabetes risk [ 46 , 47 ]. Increased glycated hemoglobin IGH is defined as a glycated hemoglobin level of 5. The diagnosis of diabetes is confirmed with a repeat test on a separate day or by the alternative test i.
Introduction
If the result of the repeat test is in the prediabetic range, the patient should be counseled or treated for pre-diabetes. If the result of the repeat test is entirely normal which is unlikely , rescreening in 6 months should be considered. One of the biggest challenges for health care providers today is addressing the continued needs and demands of individuals with chronic illnesses like diabetes [ 49 ]. The importance of regular follow-up of diabetic patients with the health care provider is of great significance in averting any long term complications.
Studies have reported that strict metabolic control can delay or prevent the progression of complications associated with diabetes [ 50 , 51 ]. Results of large randomized trials involving patients with type 1 diabetes or newly recognized or established type 2 diabetes show that control of glycemia delays the onset and slows the progression of micro vascular complications, including nephropathy, retinopathy, and neuropathy []. The needs of diabetic patients are not only limited to adequate glycemic control but also correspond with preventing complications; disability limitation and rehabilitation.
Some of the Indian studies revealed very poor adherence to treatment regimens due to poor attitude towards the disease and poor health literacy among the general public [ 55 , 56 ]. Factors that should be considered in determining glycemic goals, including psychosocial limitation [ 57 ].
In patients with severe coexisting conditions that could interfere with implementation of the management strategy, the goal is prevention of clinically significant glycosuria, water and electrolyte loss, infections, and the development of non ketotic hyperosmolar coma.