pathophysiology of DM1


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  • common illnesscommon illnesscommon illness Diabetes Mellitus is common illnessand frequently occurring illness
  • Insulin actions in peripheral tissues. Protein phosphorylation is required to mediate insulin action. After receptor autophosphorylation, the ß subunit becomes active as a tyrosine-specific kinase and catalyzes phosphorylation of several intracellular proteins. This event promotes the multifaceted actions of insulin. Insulin stimulates glucose turnover by favoring its transport across the plasma membrane followed either by oxidative or nonoxidative disposal, the latter being associated with glycogen synthesis. The effect of insulin on glucose transport is observed only in skeletal muscle, adipose cells, and heart. Insulin promotes protein synthesis in almost all tissues by virtue of a combined effect on gene transcription, messenger RNA translation, and amino acid uptake. Insulin also has a mitogenic effect that is mediated through increased DNA synthesis and prevention of programmed cell death, or apoptosis. In addition, insulin stimulates ion transport across the plasma membrane of multiple tissues. Finally, insulin stimulates lipid synthesis in fat cells, skeletal muscle, and liver while preventing lipolysis by inhibiting hormone-sensitive lipase. There is increasing evidence for a direct role of insulin, acting through the insulin or insulin-like growth factor (IGF) receptors, to regulate pancreatic ß-cell growth, survival, and insulin release from the pancreatic ß cells [],[]. Different tissues are known to respond differently to insulin. While tissue sensitivity to insulin correlates with the levels of insulin receptors expressed on the plasma membrane, it is clear that the assembly of different components of the insulin signaling pathway also confers specificity of insulin signaling on target cells. Thus, insulin-dependent glucose transport is only observed in skeletal muscle and adipose cells because these cells possess the insulin-dependent glucose transporter GLUT4. Likewise, the effect of insulin to inhibit gluconeo-genesis is specific to liver and kidney. In contrast, the effects on gene expression and protein synthesis might be ubiquitous.
  • pathophysiology of DM1

    1. 1. Type 1 Diabetes Mellitus Manoj Sharma
    2. 2. Diabetes Mellitus epidemiology • Worldwide 30 million cases in 1985 to 285 million in 2010 . • Estimated 438 million people will have DM by 2030. • T1DM accounts for 10% of all diabetics. • Incidence is increasing in most populations
    3. 3. • Incidence highest in northern european countries like Finland(35/lakh childern per year. • Africans and east asians relatively spared (0.7/lakh childern in karachi) • About 4 lakh new cases occurring annually under 14 yr world about half are in Asia. • Peak age of presentation 5-7 yr age
    4. 4. Definition A chronic disorder of carbohydrate & fat metabolism due to absolute/or relative deficiency in insulin secretion &/or ineffective biological responses to insulin resulting in hyperglycemia
    5. 5. Type 1 DM • Due to pancreatic islet B cell destruction predominantly by an autoimmune process. Immune mediated in over 90% of cases and idiopathic in less than 10% . • The rate of B cell destruction is quite variable being rapid in some individuals and slow in others
    6. 6. Insulin Promotes Anabolism Insulin lowers plasma glucose by: 1. Increasing glucose transport into most insulin sensitive cells 2. Enhancing cellular utilization and storage of glucose 3. Enhancing utilization of amino acids 4. Promoting fat synthesis
    7. 7. INSULIN
    8. 8. Glucagon Is Dominant In The Fasting State  Glucagon prevents hypoglycemia.  Glucagon is secreted when plasma glucose levels fall below 100 mg/dL.  The liver is the primary target of glucagon.  Glucagon stimulates glycogenolysis and gluconeogenesis to increase glucose output by the liver.  Glucagon release is also stimulated by plasma amino acids.
    9. 9. GLUCAGON
    10. 10. Pathogenesis of T1DM Genetic susceptibility Environmental triggers Abnormalities in immune regulation
    11. 11. Family History & Risk For Developing T1DM 0.4% occurrence rate in persons with no family history of T1DM 6-11% in offspring of person with T1DM 5% in siblings of person with T1DM 30-40% in identical twins
    12. 12. Pathogenesis of T1DM Genes Immune Regulation + Induction of Autoimmunity Beta Cell Destruction Type 1 Diabetes Environment Trigger ? Virus
    13. 13. Role of genetics • Clear familial clustering • Risk is 2% with diabetic mother but 7% when father is diabetic • Monozygotic twins concordance rate 3065% and dizygoyic twins has rate 6-10%
    14. 14. MHC/HLA encoded susceptibility to T1DM • CLASS ll genes most strongly linked • About 95% of type 1 patients possess either HLA-DR3 or HLA-DR4 alleles • Much of risk of HLA DR3/4 is because of their linkage to other alleles in DQ region.
    15. 15. Genotyping has shown haplotypes DQA1 0301 AND DQB1 0302/0201 are most strongly associated.  In addition to MHC class ll at least 20 different loci identified • Role of HLA class1 : most significant is HLA-B39.
    16. 16. • Polymorphism in promotor region of insulin gene • CTLA4 gene • Interleukin 2 and 1 receptors genes • Interferon induced helicase (lFlH1) gene • PTPN22 and PTPN2 • CYP27B1
    17. 17. Environmental Factors • Variations in urban and rural areas of same ethnic group • Change of incidence with migration • 50% of monozygotic twins are discordant for T1DM. • Increase in incidence in almost all populations in last few decades
    18. 18. Viral infections • Congenital rubella syndrome : associted with beta cell autoimmunity in 70% and development of T1DM in 40% • Viruses like coxsackie isolated post mortem from islets of some T1DM subjects • Mumps virus : possible etiology. • Rotaviruses
    19. 19. • Viral infectons can release B cell antigens • Molecular mimicry: peptide sequence of P2-C capsid of coxsackie B cross react with GAD65 in B cell membrane. • Kilham rat virus targets the animal B cells
    20. 20. Viral Replication IFIH1 Type 1 IFNs ii) Induction of Innate Immune Response & β Cell Death Viral Antigen MHC Class I i) Direct β Cell Lysis & Death Self Antigens: IAA, GAD iii) Induction of Autoimmune Response & β Cell Death l Induction of Insulitis CD8+ T-cell
    21. 21. Other Environmental factors • Early exposure to cow’s milk protien and gluten • Other dietary factors omega-3 fatty acids • Vitamin D defeciency • Zinc • Ascorbic acid • Vit E • Psychological stress
    22. 22. Pathogenesis and natural history • Initiation of autoimmunity • Preclinical autoimmunity and progressive loss of beta cell functions • Onset of clinical disease
    23. 23. • Triggers like prenatal influences, viral infection, diet in infancy are linked with onset of autoimmunity • In majority of children diagnosed before 10 years lst sign of autoimmunity appears before 02 years.
    24. 24. Initiation of autoimmunity • Most patients at diagnosis have islet cell antibodies ( ICA) are composite of several antibodies directed at pancreatic islet molecules like – Insulin antibodies(IAA) – Glutamic acid decarboxylase (GAD 65) – Tyrosine phosphatases IA-2 and IA2-b – B cell specific zinc transporter Zn-T8
    25. 25. • Risk of clnical disease increases with number of autoantibodies and intensity of response (Ab titres). • 30% risk with 1 antibody and 90% when 3 are present • ICAs serve as marker of autoimmune process of T1DM. • Assays for autoAb to GAD65 are available.
    26. 26. Autoimmunity • Strong association with endocrine and other autoimmune diseases like Schmidts syndrome • APECED- autoimmune polyendocrinopathy- candidiasis ectodermal dystrophy by mutation in AIRE gene • IPEX syndrome immunodysregulation polyendocrinopathy and enteropathy
    27. 27. Progressive loss of beta cells • Actual damage to b cells is T cell mediated and not by ICA. • Pancreatic islets are infiltirated by T and B lymphocytes, monocytes/macrophages and NK cells (insulitis) • Release of cytokines TNF a IFN g and IL1 within insulitis and progressive loss of beta cells
    28. 28. • In patients with new onset disease treatment with • anti CD3 monoclonal Ab • GAD vaccine • Anti B lymphocytes monoclonal Ab all have shown to decrease the Cpepetide levels.
    29. 29. Insulinitis Type 1 DM
    30. 30. Natural History of T1DM ? Viral Trigger β-Cell mass 100% Initiation of autoimmune response Detection of circulating autoantibodies (ICA, GAD65, IAA, IAA-2) Progressive loss of beta-cell mass induced by CD4+ & CD8+ cells Glucose < 15-20 % of intolerance β-cells are “functional” 10 remain Genetic predisposition Insulitis β-Cell injury Time (Months) Eisenbarth GS. N Engl J Med. 1986;314:1360-1368 “Pre”diabetes Diabetes
    31. 31. Pathogenesis of Type 1DM Genetic HLA-DR3/DR4 Environment ? Viral infe..?? Autoimmune Insulinitis ß cell Destruction Severe Insulin deficiency Type 1 DM
    32. 32. CONCLUSION • Increasing incidence worldwide and Asian countries accounting for about half of this number. • Clear role of genetic predisposition • Envoinmental factors like viral infections and dietery factors also important. • Autoimmunity and Progressive b cell destruction before onset of clinical disease
    33. 33. • Interplay of neural, hormonal and substrate related mechanisms leading to hyperglycemia, hyperlipedimia and eventual ketoacidosis. • About 20-40% of childern with new onset diabetes progress to DKA before diagnosis • Prediabetic phase as an opportunity to prevent subjects with active insulitis to develop clinical disease.
    34. 34. • • • • References : Oxford textbook of medicine Nelson textbook of pediatrics 19th edition Harrison’s principles of internal medicine 18th edition Lippincot’s biochemistery 5th edition
    35. 35. THANK YOU
    36. 36. TYPE 1 DIABETES MELLITUS • More recently regulatory T cell and cytotoxic T cell abnormality were considered to be critical in the development of isletitis and b cell destruction.
    37. 37. TYPE 1 DIABETES MELLITUS • The polymorphism in gene encoding cytotoxic lymphocyte antigeng4 (CTLA4) was found related to development of autoimmune diabetes as well as autoimmune thyroiditis. • B-cell reactive T cell avidity was proposed at the beginning of isletitis.
    38. 38. TYPE 1 DIABETES MELLITUS • Certain unrecognized patients with a milder expression of type 1 diabetes initially retain enough b cell function to avoid ketosis but later in life develop increasing dependency on insulin therapy as b cell mass diminishes (usually 6 years after dignosis).
    39. 39. TYPE 1 DIABETES MELLITUS • Islet cell antibody survey among northern Europeans indicate that up to 15% of “type 2”patients may actually have this mild form of type 1 diabetes (latent autoimmue diabetes of adulthood, LADA)
    40. 40. TYPE 2 DIABETES MELLITUS • This presents a heterogeneous group comprising milder forms of diabetes that occur predominantly in adults but occasionally in juveniles. • More than 90% of all diabetes in the United States and China are included under this classification . • In most cases of this type of diabetes, this cause is unkown.
    41. 41. TYPE 2 DIABETES MELLITUS • The pathogenesis currently received is illustrated in (Figure 6-18-1 ) • Tissue insensitivity to insulin has been noted in most type 2 patients irrespective of weight and has been attributed to several interrelated factors
    42. 42. Figure 6-18-1 pathogenesis of type 2 diabetes mellitus
    43. 43. TYPE 2 DIABETES MELLITUS • These include a putative(and as yet undefined ) genetic factor ,which is aggravated in time by additioal enhancers of insulin resistance such as aging ,a sedentary lifestyle, and abdominal –visceral obesity . • In addition ,there is an accompanying deficiency in the response of pancreatic b cells to glucose .
    44. 44. TYPE 2 DIABETES MELLITUS • Both the tissue resistance to insulin and the impaired b cell response to glucose appear to be further aggravated by increased hyperglycemia (glucose toxicity), and both defects are ameliorated by treatment that reduces the hyperglycemia toward normal
    45. 45. TYPE 2 DIABETES MELLITUS • Most epidemiologic data indicate strong genetic influences. • Attempts to identify genetic markers for type 2 have as yet been unsuccessful.
    46. 46. Other specific types of diabetes mellitus • Other specific types of diabetes mellitus is relatively rare • Maturity –onset diabetes of the young (MODY) is a subgroup due to monogenic disorder characterized by non-insulin – dependent diabetes with autosomal dominant inhenritantance and an age at onset of 25 years or younger.
    47. 47. Other specific types of diabetes mellitus • Diabetes due to mutant insulin is a very rare subtype of nonobese type 2 diabetes ,with no more than ten families having been described.
    48. 48. Other specific types of diabetes mellitus • Diabetes duo to a mutation of mitochondrial DNA that impairs the transfer of leucine or lysine into mitochondrial , proteins has been described.
    49. 49. Other specific types of diabetes mellitus • Since sperm do not contain mitochondria, only the mother transmits mitochondrial genes to her offspring.
    50. 50. Gestational diabetes mellitus (GDM) • GDM is defined as any degree of glucose intolerance with onset or first reconition during pregnancy. • The definition appleies regardless of whether insulin or only diet modification is used for treatment or whether the condition persists after pregnancy.
    51. 51. Gestational diabetes mellitus (GDM) • It does not exclude the possibility that unrecognized glucose intolerance may have antedated or begun concomitantly with the pregnancies. • The prevalence may range from 1%14%of pregnancies, depending on the population studied
    52. 52. Gestational diabetes mellitus (GDM) • GDM represents nearly 90% of all pregnancies complicated by diabetes. • Insulin is recommended as the only modality of treatment even trial of oral agents that are undertaken showed safe.
    53. 53. Gestational diabetes mellitus (GDM) • Deterioration of glucose tolerance occurs normally during pregnancy , particularlyi n the 3rd trimester.
    54. 54. Clinical findings • Symptoms and signs • Laboratory findings
    55. 55. Clinical findings • Symptoms and signs • The principal clinical features of the two major types of diabetes mellitus are listed for comparison in (Table 618-3)
    56. 56. Diabetes Mellitus: Signs & Symptoms Three polys: polyphagia, polyuria, & polydipsia Weight loss Fatigue Hyperglycemia
    57. 57. Clinical findings • Symptoms and signs • Patients with type 1 diabetes present with a characteristic symptom complex. • An absolute deficiency of insulin results in accumulation of circulating glucose and fat acids,with conseqent hyperosmolality and hyperketonemia.
    58. 58. Clinical findings • Symptoms and signs • Patients with type 2 diabetes may or may not present with characteristic features. • The presence of obesity or a strongly positive family history for mild diabetes suggests a high risk for the development of type 2 diabetes.
    59. 59. Laboratory findings • • • • • Urinary analysis Blood test procedures B cell Reserve Evaluation Autoantibodies Lipoprotein Abormalities in Diabetes
    60. 60. Clinical findings • Laboratory findings • Urinary analysis • Glycosuria and ketonuria can be found in diabetic patients.
    61. 61. Clinical findings • Laboratory findings • Blood test procedures • • A. Glucose Tolerance Test B. Glycated Hemoglobin (Hemoglobin A1) measurements C. Serum Fructosamine D. Self –Monitoring of Blood Glucose E.Continuous Glucose Monitoring Systems • • •
    62. 62. Blood test procedures • A. Glucose Tolerance Test • Criteria for laboratory confirmation of diabetes mellitus if the fasting plasma glucose level is 7.0 mmol/L(126mg/dL) or higher on more than one occasion , further evaluation of the patient with a glucose challenge is unnecessary .
    63. 63. Blood test procedures • A. Glucose Tolerance Test • However ,when fasting plasma glucose is less than 7.0 mmol/L(126mg/dL) in suspected cases ,a standardized oral glucose tolerance test may be ordered .
    64. 64. Blood test procedures B. Glycated Hemoglobin(HemoglobinA1) measurements Glycated hemoglobin is abnormally high in diabetics with chronic hyperglycemia and reflects their metabolic control. It is produced by nonenzymatic condensation of glucose molecules with free amino groups on the globin component of hemoglobin.
    65. 65. Blood test procedures B. Glycated Hemoglobin(HemoglobinA1) measurements The higher the prevailing ambient levels of blood glucose, the higher will be the level of glycated hemoglobin. The major form of glycohemoglobin is termed hemoglobin A1c,which normally comprises only 4%-6% of the total hemoglobin
    66. 66. Blood test procedures B. Glycated Hemoglobin(HemoglobinA1) measurements • Since glycohemoglobins circulate with in red blood cells whose life span lasts up to 120 days, they generally reflect the state of glycemia over the preceding 8-12 weeks, thereby providing an improved method of assessing diabetic control.
    67. 67. Blood test procedures B. Glycated Hemoglobin(HemoglobinA1) measurements • Measurements should be made in patients with either type of diabetes mellitus at 3-to 4 month intervals so that adjustment in therapy can be made if glycohemoglobin is either subnormal or if it is more than 2% above the upper limits of normal for a particular laboratory.
    68. 68. Blood test procedures • • C. Serum Fructosamine Serum fructosamine is formed by nonenzymatic glycosylation of serum proteins (predominantly albumin).
    69. 69. Blood test procedures • C. Serum Fructosamine • Since serum albumin has a much shorter half-life than hemoglobin, serum fructosamine generally reflects the state of glycemic control for only the preceding 2 weeks.
    70. 70. Blood test procedures • C. Serum Fructosamine • Normal values vary in relation to the serum albumin concentration and are 1.5-2.4mmol/L when the serum albumin level is 5 g/dL
    71. 71. Blood test procedures • • D.Self –Monitoring of Blood Glucose Capillary blood glucose measurements performed by patients themselves, as outpatients, are extremely useful.
    72. 72. Blood test procedures E. Continuous Glucose Monitor Systems The main value of these systems appears to be in identifying episodes of asymptomatic hypoglycemia, especially at night.
    73. 73. B cell Reserve Evaluation • It is estimated more than 50% of b cell were lost at the onset of diabetes. • The b cell reserve is usually measured in its secreted functional proteinsinsulin.
    74. 74. B cell Reserve Evalution • Measurement of insulin is usually used for functional evaluation in those not on insulin, and C-peptide can be used as an alternative toolin those on insulin. • Fasting and 2-hour after stimulator insulin or C-peptide are usually measured . • The stimulator can be glucose , arginine, glucagons.
    75. 75. B cell Reserve Evalution • Glucose is often replaced by standard meal equivalent to 75g glucose. • Reference values should be setup in each laboratory and should be interpreted according to adiposity, or insulin resistance • The evaluation is not a routine practice in clinics, but is used in research protocol.
    76. 76. Autoantibodies • It is gradually acccepted that determination of islet b cell autoimmunity is usual in typing of diabetes • Insulin autoantibody (IAA), glutamic acid decarboxylase (GADA), islet cell antibodies ( ICA) ,-now replaced by tyrosine phosphatase autoantibodies (IA-2,IA2-b) are the most commonly used tests
    77. 77. Autoantibodies • Several other antibodies were studied for their utility in predicting type 1 diabetes. • One is carboxypeptidase antibody (CPH) that is thoroughly studied a Chinese group. • IAA is more frequently detected in very young child diabetes.
    78. 78. Autoantibodies • ICA, in juvenile diabetes. • GADA, in elder diabetes. • The autoantibodies profile can change during the progression of disease. • GADA appears relatively late. • A positive result predicts the need for insulin in 6 years.
    79. 79. Lipoprotein Abnormalities in Diabetes • Circulating lipoprotein are just as dependent on insulin as the plasm glucose . • In type 1 diabetes , moderately deficient control of hyperglycemia is associated with only a slight elevation of LDL cholesterol and serum triglycerides and little if any change in HDL cholesterol
    80. 80. Lipoprotein Abormalities in Diabetes • Once the hyperglycemia is corrected, lipoprotein levels are generally normal. • However ,in obese patients with type 2 diabetes, a distict “diabetic dyslipidemia” is characteristic of the insulin resistence syndrome.
    81. 81. Lipoprotein Abormalities in Diabetes • Its feathers are a high serum triglyceride level(300-400mg/L), a low HDl cholesterol (less than 30mg/dL), and a qualitative change in LDL particles, producing a smaller dense particle whose membrane carries supro-normal amountes of free cholesterol.
    82. 82. Lipoprotein Abormalities in Diabetes • These small dense LDL particles are more susceptible to oxidation, which renders them more atherogenic. • Since primary disorders of lipid metabolism may coexist with diabetes, persistence of lipid abnormalities after restoration of normal weight and blood glucose should prompt a diagnostic workup and possible pharmacotherapy of the lipid disorder.
    83. 83. Differential Diagnosis • Hyperglycemia secondary to other sources • Secondary hyperglycemia has been associated with various disorders of insulin target tissues (liver, muscle , and adipose tissue)(Table 6-18-5).
    84. 84. Differential Diagnosis • Other secondary cause of carbohydrate intolerance include endocrine disorders-often specific endocrine tumors-accociated with excess production of growth hormone, glucocorticoids, catecholamines, glucagon , or somatostatin.
    85. 85. Differential Diagnosis • A rare syndrome of extreme insulin resistance associated with acanthosis nigricans afflicts either young women with androgenic features as well as insulin receptor mutations or older people , mostly women , in whom a circulating immunoglobulin binds to insulin receptors and reduces their affinity to insulin.
    86. 86. Differential Diagnosis • Medications such as diuretics , phenytoin , niacin, and high-dose glucocorticoids can produce hyperglycemia that is reversible once the drugs are discontinued or when diuretic-induced hypokalemia is corrected
    87. 87. Differential Diagnosis • Chronic pancrearitis or subtotal pancreatectomy reduces the number of functioning b cells and can result in metabolic derangement very similar to that of genetic type 1 diabetes except that a concomitant reduction in pancreatic a cells may reduce glucagon secretion so that relatively lower doses of insulin replacement are needed.
    88. 88. Differential Diagnosis • Insulin-dependent diabetes is occassionally associated with Addison’s disease and autoimmune thyroiditis (Schimidt’s syndrome, or polyglandular failure syndrome).
    89. 89. Differential Diagnosis • This occurs more commonly in women and represents an autoimmune disorder in which there are circulating antibodies to adrenocortical and thyroid tissue, thyroglobulin,and gastric parietal cells.
    90. 90. Nondiabetic Glycosuria • Nondiabetic glycosuria(renal glycosuria) is a benign asymptomatic condition wherein glucose appears in urine despite a normal amount of glucose in blood , either basally or during a glucose tolerance test.
    91. 91. Nondiadetic Glycosuria • Its cause may vary from an autosomally transmitted genetic disorder to one associated with dysfunction of the proximal renal tubule (Fanconi’s syndrome ,chronic renal failure), or it may merely be a consequence of the increasd load of glucose presented to the tubules by the elevated glomerular filtration rate during pregnancy.
    92. 92. Nondiabetic Glycosuria • As many as 50% of pregnant women normally have demonstrable sugar in the urine, especially during the third and fourth months. • This sugar is practically always glucose except during the late weeks of pregnancy , when lactose may be present.
    93. 93. Treatment • Diabetes mellitus requires ongoing medical care as well as patient and family education both to prevent acute illness and to reduce the risk of longterm complications.
    94. 94. Treatment • Diet • A well-balanced , nutritious diet remains a fundamental element of therapy. • However, In more than half of case ,diabetic patients fail to follow their diet . • In prescribing a diet, it is important to relate dietary objectives to the type of diabetes.
    95. 95. Treatment • Diet • In obese patients with mild hyperglycemia, the major goal of diet therapy is weight reduction by caloric restriction. • Thus ,there is less need for exchange lists, emphasis on timing of meals ,or periodic snacks, all of which are so essential in the treatment of insulin – requiring nonbese diabetics.
    96. 96. Treatment • ADA Recommendations • The American Diabetes Association release an annual position statement on medical nutrition therapy that replaces the calculated ADA diet formula of the past with suggestions for an individully tailored dietary prescription based on metabolic , nutritional, and life style requirements .
    97. 97. Treatment • ADA Recommendations • They contend that the concept of one diet for “diabetes” and the prescription of an “ADA diet” no longer can apply to both major type of diabetes. • In their recommendations for persons with type 2 diabetes, the 55%-60% carbohydrate content of previous diets has been reduce considerably because of the tendency of high carbohydrate intake to cause hyperglycemia, hypertriglyceridemia, and a lowered HDL cholesterol
    98. 98. Treatment • ADA Recommendations • .In obese type 2 patients, glucose and lipid goals join weight loss as the focus of therapy . • These patients are advised to limit their carbohydrate content by substituting noncholesterologenic monounstaturated oils such as olive oil ,rapeseed (canola) oil, or the oil in nuts and avocados.
    99. 99. Treatment • ADA Recommendations • This maneuver is also indicated in type 1 patients on intensive insulin regimens in whom near-normoglycemic control is less achievable on higher carbohydrate diets.
    100. 100. Treatment • ADA Recommendations • They can administer 1 unit of regular insulin or insulin lispro for each 10 or 15 g of carbohydrate eaten at a meal . • In these patients , the ratio of carbohydate to fat will vary among individuals in relation to their glycemic responses ,insulin regiments, and exercise pattern.
    101. 101. Treatment • ADA Recommendations • The current recommendations for both types of diabetes continue to limit cholesterol to 300 mg dairly and advise a daily protein intake of 10%-20% of total calories
    102. 102. Treatment • ADA Recommendations • They suggest that saturated fat be no higher than 8%-9% of total calories with a similar proportion of polyunsaturated fat and that the remainder of caloric needs be made up of an individualized ratio of monounsaturated fat and of carbohydrate containing 20-35 g of dietary fiber .
    103. 103. Treatment • ADA Recommendations • Poultry ,veal, and fish continue to be recommended as a substitute for red meats for keeping saturated fat content low. • The present ADA position statement proffers no evidence that reducing protein intake below 10% of intake (about 0.8 g/kg/d) is of any benefit in patients with nephropathy and renal impairment ,and doing so may be detrimental.
    104. 104. Treatment • Dietary Fiber • Plant components’ such as cellulose ,gum, and pectin are indigestible by humans and termed dietary “fiber”. • The ADA recommends food such as oatmeal , cereals, and beans with relatively high soluble fiber content as staple components of the diet in diabetics.
    105. 105. Treatment • Dietary Fiber • High soluble fiber content in the diet may also have a favorable effect on blood cholesterol levels.
    106. 106. Treatment • Artifficial Sweeteners • The latest position statement of ADA concludes that all nonnutritive sweeteners that have been approved by the FDA (such as aspartame and saccharin) are safe for consumption by all people with diabetes.
    107. 107. Treatment • Artifficial Sweeteners • Two other nonnutritive sweeteners have been approved by the FDA as safe for general use: sucralose(Splenda) and acesulfame potassium (Sunett ,Sweet one, DiabetiSweet)
    108. 108. Treatment • Artifficial Sweeteners • Nutritive sweeteners such as sorbitol and fructose have increased in popularity . • Except for acute diarrhea induce by ingestion of large amounts of sorbitol – containing foods, their relative risk has yet to be established.
    109. 109. Treatment • Artifficial Sweeteners • Fructose represents a “natural ”sugar substance that is a highly effective sweetener which induces only slight increases potential adverse effects of large amounts of fructose (up to 20% of total calories) on raising serum cholesterol and LDL cholesterol , the ADA feels it may have no overall advantage as a sweetening agent in the diabetic diet.
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