Clin Chem LEC Module 5 Carbohydrates PDF

Kristelle Anne Diadio BSMLS 3B asymmetric carbon forming molecules Clin Chem LEC called stereoisomers...

Kristelle Anne Diadio BSMLS 3B asymmetric carbon forming molecules Clin Chem LEC called stereoisomers  Stereoisomers - same order and types of bonds but different spatial arrangements For each asymmetric carbon there MODULE 5 are 2n possible isomers  A monosaccharide is assigned to Carbohydrates the D or the L series according to the configuration at the highest umbered asymmetric carbon (configuration atom or chiral CARBOHYDRATES center) If the hydroxyl group  Carbohydrates - Primary source of energy for brain, projects to the right: D-series erythrocyte, and retinal cells in humans Hydroxyl group to the left: L- Major food source and energy supply of the body series and are stored primarily as liver and muscle These stereoisomers are glycogen called enantiomers Provide structural integrity to the cell membrane  Enantiomers - images that are not superimposable Compounds containing carbon, hydrogen, and with each other (mirror-image) oxygen joined together to form molecules  Most sugars in humans are in the D-form Contains carbonyl and hydroxyl functional groups o Classified based on the following properties: 1. Size of the base carbon chain Another classification is based on number of 2. Location of the carbonyl (CO) functional group sugar units in the chain: 3. Number of sugar units 1. Monosaccharides - Cannot be hydrolyzed to a 4. Stereochemistry of the compound simpler form Examples: Glucose (dextrose), Fructose (levulose), Galactose CLASSIFICATION OF CARBOHYDRATES 2. Disaccharides - Formed when 2 monosaccharide units are joined by a glycosidic linkage, with the  Can be grouped based on the number of production of water carbons in the molecule: Can be hydrolyzed into two monosaccharides by 1. Trioses - Contains three (3) carbon atoms disaccharide enzymes Examples: smallest carbohydrate: glyceraldehyde Examples: Sucrose, Lactose, and Maltose 2. Tetroses - Contains four (4) carbon atoms 3. Pentoses - Contains five (5) carbon atoms Another classification is based on number of Examples: ribose, deoxyribose sugar units in the chain: 4. Hexoses - Contains six (6) carbon atoms 1. Oligosaccharides - Chaining of 2 to 10 sugar units Examples: simple sugars (glucose, galactose, fructose) 2. Polysaccharides - Linkage of many monosaccharide units  Hydrates of aldehyde or ketone derivatives On hydrolysis, will yield more than 10 based on the location of the carbonyl (CO) monosaccharides functional group: Examples: Starch (glucose molecules), glycogen, cellulose, 1. Aldose - Forms a terminal and chitin carbonyl group called an aldehyde group GLUCOSE METABOLISM 2. Ketose - Forms a carbonyl group in the middle linked to two other  Most of our ingested carbohydrates are polymers, such carbon atoms called ketone group as starch or glycogen, sucrose, lactose, and cellulose  Salivary amylase - converts starch into dextrins, Stereoisomers maltose, and glucose  Central carbons of CHO are asymmetric (chiral)  Fate of glucose: This allows for various spatial 1. CHO digestion starts in the mouth where the enzyme arrangements around each salivary amylase is secreted by the salivary gland  Kristelle Anne Diadio BSMLS 3B 2. In the stomach, amylase activity is halted because of the  Pathways in glucose metabolism: acidity of the environment 1. Glycolysis - Breakdown of glucose to pyruvate or The HCl produced by the parietal cell of the stomach lactate is responsible for the acidity 2. Gluconeogenesis - Breakdown of amino acids 3. CHO digestion is continued when the chyme reaches the (alanine) to form glucose-6-phosphate duodenum of the small intestines 3. Glycogenolysis - Breakdown of glycogen to glucose 4. These products are then acted upon by disaccharidases 4. Glycogenesis - Conversion of glucose to glycogen for located in the brush border of the cells lining the lumen storage of the small intestines Cellulose remains unchanged and is eventually 5. Lipogenesis - Conversion of CHO to fatty acid excreted via stool 6. Lipolysis - Decomposition of fats Some of the monosaccharides are absorbed by the intestines Glucose and galactose are absorbed from the lumen HORMONES THAT REGULATE GLUCOSE of the intestines by an active process involving co- HOMEOSTASIS transport with sodium 5. The monosaccharide reaches the liver via the portal  Pancreas - Both an endocrine and exocrine organ circulation, interconversion of hexoses occurs As an exocrine gland, it produces and secretes an This process ensures conversion of fructose and amylase responsible for the breakdown of ingested galactose into glucose complex carbohydrates 6. After the interconversion process, the liver dispatches As an endocrine gland, it secretes the hormones the glucose molecules to the different extrahepatic insulin, glucagon, and somatostatin from different tissues in need of an energy source cells residing in the Islets of Langerhans 7. Glucose enters the glycolytic pathway or the Embden- Meyerhof pathway which extracts energy from glucose (1) Insulin and converts it in the form of Adenosine Triphosphate  Insulin - Produced by the beta cells of the Islets of (ATP) Langerhans of the pancreas as a prohormone called 8. Glucose is stored in the liver as glycogen pro-insulin; Primary hormone responsible for the entry of glucose into the cell  During starvation, when the tissues run out of glucose o Functions: fuel, the glycogen stores from the liver are mobilized 1. Stimulates glucose uptake and glycogen formation  The glycogen reserve, is only about 100 g 2. Inhibits glucose production in insulin-sensitive After about 10-18 hours of fasting, it becomes tissues which includes liver, skeletal muscles, and depleted adipose tissues  To further maintain the blood glucose level within  A peptide hormone having a mass of approximately normal the muscle proteins must be mobilized 5000 Daltons  Proteins are degraded to form amino acids, many of  Possesses 21 aa A chain and 30 aa B chain linked which are glucogenic: they can be converted into together by disulfide bonds glucose o Proinsulin is seen in:  The amino acids produced, particularly alanine, are 1. Type 2 diabetes with decreased ability of beta cells brought to the liver where they are converted into to secrete insulin glucose, a process called gluconeogenesis 2. Pre Type 1 diabetes  Fatty acids are also brought to the liver where they are 3. Insulinomas converted to acetyl CoA, the precursor of ketone bodies 4. Familial hyperinsulinemia Ketone bodies - serve as an important source of energy for many vital organs including the brain & the  Proinsulin - is processed by cleavage to form C- heart especially in cases of starvation peptide and insulin  Ratio of C-peptide to insulin is 5:1 to 15:1 in serum Regulation of carbohydrate metabolism  C-peptide has become a marker for endogenous production of insulin to differentiate it from o The liver plays a major role: administration of exogenous insulin 1. The release of absorbed glucose for the cells Measured in conjunction with insulin and blood immediate energy needs glucose to help identify cause of hypoglycemia 2. Conversion of non-CHO substances to glucose 3. Conversion of excess glucose into glycogen 4. Breaking down of stored glycogen to glucose  Kristelle Anne Diadio BSMLS 3B Relationship of C-peptide and insulin levels in different 3. Effects on Protein Synthesis - Insulin stimulates the hypoglycemic states entry of amino acids into the cells Conditions Insulin Level C-peptide Level It also promotes synthesis of protein in most tissues Insulinoma Increased Increased Insulin treatment Increased Decreased Type I Diabetes Absolute deficiency Decreased o Action of insulin: 1. Increases glycogenesis, lipogenesis, and glycolysis 2. Decreases glycogenolysis  To follow-up evaluations after pancreatectomy  C-peptide and proinsulin are primarily degraded by the kidneys Interferences in measurement of insulin, C- peptide, & proinsulin:  Insulin secretion is stimulated by the following 1. Hemolysis factors: Insulin: falsely decreased C-peptide: less affected 1. Glucose - The most important stimulus of insulin Proinsulin: less affected production 2. Insulin antibodies This happens after a meal rich in carbohydrates Insulin: falsely increased/decreased 2. Amino Acids - A.A. particularly arginine stimulate the B cell to secrete insulin; Occurs after a protein rich meal  Clinical significance of changes in insulin levels: 3. Gastrointestinal hormones - The intestinal peptide 1. Insulin deficiency (absolute or relative): Diabetes secretin and other GI hormones stimulate the mellitus secretion of insulin 2. Increased insulin secretion: a. Insulin-resistant patients These hormones are released usually after b. Increased insulin with decreased glucose level ingestion of food suggests inappropriate secretion or administration They cause anticipatory rise in the insulin levels of insulin before actual rise of blood glucose 3. Unregulated excessive insulin secretion: a. Seen in insulinomas  The metabolic effects of insulin are prominent in b. Patients show decreased glucose < 50 mg/dL the liver, muscles, and adipose tissue: c. Hypoglycemic 1. Effects on CHO Metabolism In the liver: insulin decreases production of glucose (2) Glucagon by inhibiting gluconeogenesis and glycogenolysis In the muscle and liver: insulin increases  Glucagon - A polypeptide hormone secreted by the glycogenesis alpha-cells of the pancreatic Islets of Langerhans, In the muscle and adipose tissue: insulin increases released during stress and fasting states glucose uptake Acts by increasing plasma glucose levels by o The increased glucose uptake has been attributed glycogenolysis and gluconeogenesis to the ability of the insulin to bind with its It has only 1 target, the liver: increases hepatic receptor on these cells and trigger the increase in lipolysis the number of glucose transporters in the cell o Thus, there is an increase in glucose and fatty membrane (GLUT-4 which is very rich in the acids muscles and adipose tissues) Normal concentration: 25-50 pg/mL 2. Effects on Lipid Metabolism - The immediate effect o Functions: of insulin in lipid metabolism is the decrease in FA 1. Stimulates glucose production that is mediated by levels the generation of cAMP Insulin decreases triglyceride degradation (lipolysis) 2. Regulates/activates hepatic glycogenolysis, in the adipose tissues gluconeogenesis, and ketogenesis o It is done by inhibiting the hormone-sensitive 3. Primary hormone responsible for increasing lipase present in adipose tissues glucose levels It promotes triglyceride synthesis by increasing transport of glucose into the adipocytes providing  Proglucagon and its products: the glycerol-3-phosphate needed in triglyceride 1. Proglucagon is produced by: synthesis a. Pancreatic alpha cells Insulin increases the activity of the lipoprotein b. L cells of the distal small bowel lipase or lipemia clearing factor in the plasma 2. Glucagon - Results from the differential processing of proglucagon  Kristelle Anne Diadio BSMLS 3B 3. GLP-1 (Glucagon-like peptide) - Formed from c. Acromegaly o Pancreatitis glucagon d. Renal insufficiency It functions as incretin that stimulates insulin e. Patients with multifunctional neuroendocrine secretion after a meal tumors Suppression of glucagon and lipase secretion; f. Familial hyperglycemia inhibition of gastric emptying and stimulation of somatostatin (3) Epinephrine  Epinephrine - Produced by the adrenal medulla  Glucagon secretion is stimulated by the Activates the adenylate cyclase which produces following factors: cyclic adenosine monophosphate (cAMP) 1. Low blood glucose - a primary stimulus for glucagon Increased levels of cAMP activate the enzyme secretion phosphorylase causing increased glycogenolysis During an overnight fast, elevated glucagon levels It also stimulates the breakdown of TAG by prevent hypoglycemia activating the hormone sensitive lipase of 2. Amino acids - stimulate the release of both glucagon adipocytes and insulin Inhibits insulin secretion and insulin-dependent It prevents hypoglycemia that would otherwise uptake of glucose by peripheral tissues occur as a result of increased insulin secretion after Released during times of stress a protein meal 3. Epinephrine - produced by the adrenal medulla; (4) Somatostatin stimulates the release of glucagon  Somatostatin - Produced by the delta cells of the During periods of stress, trauma, and excessive Islets of Langerhans of the pancreas exercise the elevated epinephrine causes elevation Comprises 5-10% of the Islet cells of glucagon in anticipation of increased glucose use Inhibits both insulin and glucagon secretion and In contrast, insulin levels are depressed secretion of other hormones Inhibits the action of insulin, glucagon, and growth  Metabolic effects of glucagon include the hormone following:  Clinical significance: Increased in: somatostatinoma, 1. Effects on CHO metabolism - Leads to an increase in medullary thyroid cancer, small cell lung cancer, and blood sugar due to breakdown of liver glycogen and pheochromocytoma an increased gluconeogenesis 2. Effects on Lipid metabolism - Favors hepatic (5) Cortisol oxidation of fatty acids and subsequent formation of ketone bodies from acetyl CoA  Cortisol - A glucocorticoid produced by the adrenal cortex The lipolytic effect of glucagon in adipose tissue is minimal in humans Produced upon stimulation of the adrenal cortex by the adrenocorticotrophic hormone (ACTH) 3. Effects on Protein metabolism - Glucagon increases produced by the anterior pituitary gland the uptake of amino acids by the liver resulting in Its main activity is to stimulate gluconeogenesis and increased availability for carbon skeletons needed for lipolysis gluconeogenesis It promotes protein catabolism and deamination As a consequence, plasma levels of amino acids are It inhibits glucose metabolism in the peripheral decreased tissues  Clinical significance of changes in glucagon (6) Growth hormone levels: 1. Glucagon deficiency results in:  Growth hormone - Produced by the anterior pituitary a. Increased glycemic fluctuations gland b. Difficulty in recovering from hypoglycemia It has an antagonistic action to insulin (Insulin 2. Excessive glucagon increase: increases the entry of glucose into the cell, while a. Excessive increase is seen in glucagonomas growth hormone decreases the entry of glucose b. Fasting glucagon level is >120 pg/mL with levels into the cell) ranging from 900 to 7800 pg/mL It inhibits uptake of glucose by the cells and 3. Mild elevations are seen in: lipogenesis from carbohydrates a. Cirrhosis o Diabetes Promotes the release of fatty acids from adipocytes b. Cushing’s syndrome  Kristelle Anne Diadio BSMLS 3B (7) Thyroid hormone 2.50-55 mg/dL observable symptoms 3.Blood glucose level of less than 50 mg/dL in infants  T3 and T4 - promote the absorption of glucose in the is considered abnormal and requires diagnostic intestinal tract treatment They also stimulate glycogenolysis and accelerates 4. Diagnosed in a first week old baby if the level is the degradation of insulin less than 25 mg/dL In effect, they increase glucose levels in the blood 5. Pre-term or low birth weight infant: < 35 mg/dL 6. Full-term infants: < 45 mg/dL from birth to the (8) Human Placental Lactogen first 72 hours thereafter  Human Placental Lactogen - Derived from placenta  Classic symptoms of hypoglycemia: Confusion, Insulin antagonist (thus causes an increase in dizziness, unconsciousness, seizures, palpitations, glucose level) tremors, hunger, weakness, anxiety, fatigue, blurred vision, diplopia, tingling, nightmares, mental disturbances, diaphoresis CLINICAL CONDITIONS OF CARBOHYDRATE o Classification of hypoglycemia: METABOLISM 1. Drug administration 2. Critical illness (1) HYPERGLYCEMIA 3. Hormonal deficiency 4. Endogenous hyperinsulinism  Hyperglycemia - An increase in blood glucose 5. Autoimmune hypoglycemia concentration 6. Non-beta cell tumors FBS level: >126 mg/dL 7. Hypoglycemia of infancy and childhood o Causes: 8. Alimentary (reactive) hypoglycemia 1. stress 9. Idiopathic (functional) postprandial hypoglycemia 2. severe infection 3. dehydration or pregnancy  Symptoms of hypoglycemia can be divided into 4. pancreatectomy two categories: 5. hemochromatosis 6. insulin deficiency, or abnormal insulin receptor 1. Adrenergic symptoms - Mediated by epinephrine o Lab findings: release as regulated by the hypothalamus in 1. increased glucose in plasma and urine response to hypoglycemia 2. increased urine specific gravity Includes anxiety, weakness, palpitation, tremor, and 3. ketones in serum and urine sweating 4. decreased blood and urine pH (acidosis) They usually occur when blood glucose falls 5. electrolyte imbalance (decreased Na, increased K, abruptly decreased HCO3) 2. Neuroglycopenic symptoms - Due to impaired delivery of glucose to the brain Includes headache, confusion, slurred speech, (2) HYPOGLYCEMIA seizures, coma, and death  Hypoglycemia - Characterized by low or decreased Results from gradual decline in glucose, often levels plasma glucose level below 40 mg/dL It results from an imbalance between glucose o Deprives the CNS of fuel but fails to trigger utilization and production epinephrine release The warning signs and symptoms are related to CNS o Patient must meet the criteria of Whipple’s Triad:  Classification of hypoglycemia: 1. Low blood glucose concentration 1. Post-prandial (Reactive) hypoglycemia - More 2. Typical symptoms of hypoglycemia common; There is exaggerated insulin release 3. Symptoms relieved promptly by administration of following a meal, prompting transient hypoglycemia glucose with mild adrenergic symptoms  Glucose Tolerance Test - should be performed with Plasma glucose level results return to normal even great caution in patients with suspected when the patient is not fed hypoglycemia because the procedure can induce o The only treatment usually required is that the severe reactive hypoglycemia causing loss of patient eat frequent small meals rather than 3 consciousness and even shock large meals  Diagnostic test: 5-hour glucose tolerance test 2. Fasting hypoglycemia - Rare but most serious; o Hypoglycemic values: Neuroglycopenic symptoms are common and it may 1. < 60 mg/dL strongly suggests hypoglycemia  Kristelle Anne Diadio BSMLS 3B result from decreased rate of glucose production by (B) Type 2 Diabetes Mellitus the liver  Type 2 Diabetes Mellitus - Characterized by Decreased blood glucose levels are usually seen in hyperglycemia that results from insulin resistance patients with hepatocellular damage or adrenal with an insulin secretory defect insufficiency (decreased cortisol) There is relative insulin deficiency Constitutes the majority of diabetes cases (3) DIABETES MELLITUS  Risk factors: Obesity, lifestyle, family history, lack of  Diabetes Mellitus - A group of metabolic disease exercise, history of gestational DM, impaired glucose characterized by hyperglycemia resulting from metabolism, hypertension, dyslipidemia defects in insulin secretion or due to abnormal insulin  Associated with strong genetic predisposition and not action or both related to an autoimmune disease Vital organs affected: eyes, kidneys, and heart  Described as a geneticist’s nightmare o Complications:  The individuals are at risk of developing macrovascular 1. End stage renal disease and microvascular complications 2. non-traumatic amputation  Has milder symptoms as compared to Type 1 DM 3. adult blindness  Untreated Type 2 DM will result to nonketotic 4. diabetic neuropathy hyperosmolar coma due to overproduction of glucose (> 5. atherosclerotic disease 300 mg/dL) accompanied by severe dehydration, 6. heart attacks electrolyte imbalance and increased BUN and creatinine 7. strokes  Insulin resistance - Occurs when tissues fail to o Three classic manifestations of Diabetes Mellitus: respond normally to insulin 1. Polyuria - Excessive urination 2. Polydipsia - Excessive thirst  The insulin resistance could be: 3. Polyphagia - Excessive hunger 1. Pre-receptor - The insulin could be defective that it has difficulty binding with its receptors on the target (A) Type 1 Diabetes Mellitus cells or the levels of insulin may be low  Type 1 Diabetes Mellitus - Due to an absolute 2. Receptor - The patient fails to respond to insulin deficiency of insulin caused by massive autoimmune because the receptors may be deficient or defective attack of the beta-cells of the pancreas 3. Post-receptor - The patient has normal levels of Causes hyperglycemia, ketoacidosis, and insulin or receptors but signal transduction cannot hypertriglyceridemia occur or another possibility is the inability to process o Causes of Type 1 DM: glucose transporters leading to decreased uptake of 1. Viral infection and environmental factor glucose by the cells 2. Genetic susceptibility (HLA DR3/DR4 on chromosome no. 6) TYPE I (IDDM) TYPE II (NIDDM) Synonyms Juvenile-onset DM, Adult-onset DM, 3. Stress Brittle diabetes, Ketosis- Maturity-onset DM,  Complications: nephropathy, neuropathy, retinopathy prone DM Stable diabetes, Ketosis-  Idiopathic Type 1 DM - No known etiology, strongly resistant DM, Receptor- deficient DM inherited, episodic requirement for insulin Pathogenesis Beta-cell destruction Insulin resistance replacement Incidence Rate 5-10% 90-95% Onset Any; most common to Any; most common with Ketones childhood/teens advancing age C-peptide Decreased or Detectable  Ketones - Produced by the liver levels undetectable o 3 ketone bodies: Pre-diabetes (+) Autoantibodies (-) Autoantibodies Ketosis Common; poorly Rare 1. Acetone controlled 2. Aceto-acetic acid Medication Insulin absolute Oral agents 3. Beta-hydroxybutyric acid  In severe DM, the ratio of beta-hydroxybutyric acid to  Endocrinopathies in Diabetes Mellitus: aceto-acetic acid is 6:1 (normal is 1:1) 1. Cushing’s syndrome - Excessive production of  Factors which stimulate production of ketones: cortisol Starvation, high fat diet, prolonged vomiting, glycogen 2. Pheochromocytoma - Tumor affecting chromaffin cells storage disease Excessive production of catecholamines 3. Acromegaly - Excessive enlargement of bones Excessive production of growth hormone  Kristelle Anne Diadio BSMLS 3B 3. Diabetes Mellitus = greater than or equal to 126 (C) Gestational Diabetes mg/dL o Categories of Oral Glucose Tolerance Test:  Gestational Diabetes - A disorder characterized by 1. Normal/Non-diabetic = 2-hr plasma glucose (PG) < impaired ability to metabolize carbohydrates usually 140 mg/dL caused by insulin deficiency, metabolic or hormonal 2. Impaired GTT = 2-hr PG 140-199 mg/dL changes 3. Diabetes mellitus = 2-hr PG ≥ 200 mg/dL Occurs during pregnancy and disappears after o Diagnostic criteria for DM: delivery, in some cases, after 5-10 years it develops 1. RBS = ≥200 mg/dL (with symptoms of DM) into Type 2 DM 2. FBS = ≥126 mg/dL Screening of GDM should be performed between 3. 2-hr Post Glucose Load = ≥200 mg/dL 24 to 48 weeks of gestation 4. HbA1c = ≥6.5 % The screening and diagnosis of GDM is by performance of a 2-hour OGTT using 75-gram  Samples for Glucose Measurement: glucose load 1. RBS (Random Blood Sugar) - Requested during o Diagnostic criteria for GDM: insulin shock and hyperglycemic ketonic coma 1. FBS - greater than or equal to 92 mg/dL Blood glucose taken any time of the day and 2. 1 hour GCT - greater than or equal to 180 mg/dL without fasting 3. 2 hour OGTT - greater than or equal to 153 mg/dL Often used for emergency cases  GDM is diagnosed if one of the three criteria is met 2. FBS (Fasting Blood Sugar) - Measure of overall  Infants born to diabetic mothers are at increased risk for respiratory distress syndrome, hypocalcemia, and glucose homeostasis hyperbilirubinemia Requirement: NPO at least 8 hours before the test  After giving birth, women with GDM should be Usually done in the morning to prevent diurnal evaluated 6 to 12 weeks postpartum variation  GDM converts to DM within 10 years in 30%-40% of 3. 2-hour PPBS (Post-Prandial Blood Sugar) - It cases measures how well the body metabolizes glucose 4. OGTT (Oral Glucose Tolerance Test) - Multiple blood glucose test GLUCOSE METHODOLOGIES Used to determine how well the body metabolizes glucose over a required period of time, same with Specimen Consideration and Patient Preparation 2-HPPBS  Standard clinical specimen: fasting venous plasma Should be performed to diagnose GDM  Fasting glucose in whole blood is 15% lower than in serum/plasma  Kinds of Glucose Tolerance Tests:  Serum is appropriate for glucose analysis if it is 1. Oral Glucose Tolerance Test (OGTT) separated from the cells within 30-60 minutes Types of OGTT:  Venous blood glucose is 7 mg/dL lower than capillary a. Janney-Isaacson Method (Single Dose Method) – blood due to tissue metabolism; capillary blood glucose most common is same with arterial blood glucose b. Exton Rose Method (Divided Oral Dose/Double  CSF glucose concentration should be approximately 60% Dose Method) of plasma concentration Requirements/Guidelines for OGTT:  At room temperature, glucose is metabolized at a rate a. Patient should be ambulatory of 7 mg/dL/hour b. Fasting for 8-14 hours  At refrigerated temperature (4 deg C), glucose is c. Unrestricted diet of 150g of CHO per day for days metabolized at a rate of about 2 mg/dL/hour prior to testing  2 mg of sodium fluoride (NaF) per mL of whole blood d. Patient should not smoke and drink alcohol prior to prevents glycolysis for up to 48 hours testing  Fluoride - binds magnesium, which causes inhibition e. Glucose load: of the enzyme enolase (1) 75 grams (WHO standard) (2) 100 grams (3) 1.75 g of glucose per kg body weight (children, Diagnostic Criteria max of 75 g) o Criteria for Fasting Plasma Glucose (FPG): 2. Intravenous Glucose Tolerance Test (IVGTT) - It is 1. Non-diabetic (Prediabetes) =