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Exam 1 Notes

by: Channelle Brown

Exam 1 Notes HUN3224

Channelle Brown

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Exam 1 material which covered carbohydrates, diabetes, and the GI tract. Also includes all the pathways and diagrams.
Intermediary Metabolism
Dr. Farrell
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This 33 page Bundle was uploaded by Channelle Brown on Saturday April 23, 2016. The Bundle belongs to HUN3224 at Florida State University taught by Dr. Farrell in Spring 2016. Since its upload, it has received 41 views. For similar materials see Intermediary Metabolism in Nutrition and Food Sciences at Florida State University.

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Date Created: 04/23/16
GI Tract – HUN3224  Most of immune system is in GI tract  Oral Cavity o Mastication – chewing breaks down food  Increases surface area o Saliva  Enzymes  Salivary amylase – carbs  Salivary lipase – milk fat (most active in infants)  Lysozymes  Kill bacteria  Our first defense  Esophagus o Muscular tube – connect the back of the mouth and stomach  Movement of food via peristalsis o Lower esophageal sphincter – circular muscular valve  Relaxes to let food into stomach  Constricts to keep food from moving back up into esophagus o GERD (gastro esophageal reflux disease)  Relaxation of LES (weak LES)  Stomach acid comes in contact with esophagus  Possible causes: spicy foods, caffeine, fatty foods, pregnancy, pressure from obesity, laying down after eating, etc.(  Over time can damage esophagus leading to ulcers and an increased of esophageal cancer  Stomach o Holds food o Mechanical mixing and breaking down of food o Gastric secretions  Gastrin  Release of HCl and pepsinogen  Hydrochloric Acid (HCl)  Kill bacteria  Denatures proteins  Inactivates lingual lipase  Converts pepsinogen into pepsin  Pepsinogen  Inactive precursor to pepsin *all proteases are inactive at rest*  Protein digestion  Mucus  Protects stomach lining  Contains bicarbonate to neutralize acid  Intrinsic Factor  Necessary for absorption of B12  Lack of B12 – anemia, lethargy, etc. o Absorption of alcohol and aspirin  Pyloric Sphincter o Circular muscular valve separating stomach from duodenum o Regulates movement of food and acid from stomach to small intestine o If it does not work properly”dumping”diarrhea o Chime = food + acid  Small Intestine o 3 sections:  Duodenum  Main site of digestion and absorption  Receives secretions from other digestive organs (pancreas, gallbladder)  Lining: folded into finger-like projections called villi o Increases surface area, increases absorption o Villi – covered with microvilli o Microvilli = brush border (where digestion is usually completed) o Villi are lined with enterocytes (“gate keepers”)  Villar tip cells – slough off (the tip)  Midvillar cells – secrete digestive enzymes & hormones for macronutrient digestion (CCK, secretin, GIP)  Crypt cells – replicate (bottom)  Jejunum  Digestion and absorption continue  Ileum (longest section)  Absorption  Enterohepatic circulation of bile  We reabsorb most bile  Large Intestine o Smooth lining, no villi o Water and electrolyte absorption o Intestinal microflora – bacterial breakdown of fiber; produce vit. K and some B vitamins  When we are born, we get a shot of Khelps us produce bacteria in gut o Temporary storage and concentration until defecation  Accessory Organs o Pancreas  Acini – secrete enzymes into GI tract  Zymogens  Pancreatic amylase  Pancreatic lipase  Islet tissue  Secrete hormones into blood o Beta – insulin o Alpha – glucagon o Delta – somatostatin  Not connected to GI  Shares common bile duct with gallbladder gallstoneback system uppancreatitisimbalance of blood glucose o Liver  Makes bile  Emulsifier for fats, needed for fat digestion  Bile o Made in hepatocytes from cholesterol o Stored in gallbladder o After digestion of fats, bile reabsorbed in ileum and sent back to liver (EHC)  Metabolizes drugs, alcohol, and toxins  Urea synthesis  Makes plasma proteins  Transport proteins o Albumin: maintains osmotic pressure; low albuminfluid pools in intercellular spaces = edema o Transferrin : transports iron o Lipoproteins: 5 types (chylomicron, VLDL, IDL, LDL, HDL), carries various lipid/cholesterol components to tissues  Circulation of Nutrients o Vascular System  Carries nutrients in blood to liver and then disperses it to body (EHC)  For water-soluble substances o Lymph System  Exogenous lipid transport  Lacteals (fat/fat-soluble substances go through these)  Fatdirectly into bloodstream Carbohydrates – HUN3224  Major source of energy fuel in average diet  ½ total caloric intake o Polysaccharides (starches & dextrins) o Monosaccharides (simple sugars – glucose, galactose, fructose) o Some are digestible, some are not  Chemical structure (below: most simple carb) o Simple: glyceraldehyde o Complex: glycogen  Monosaccharides o Types (based on # of carbons)  3 – triose  4 – tetrose  5 – pentose (made from hexoses; helps made riboses)  6 – hexoses (major energy source: glucose, galactose, fructose)  7 – heptose  Dietary Monosaccharides (“simple carbs”) o Glucose  Most abundant of the three  “blood sugar” o Fructose o Galactose  Disaccharides o Formed from condensation of 2 monosaccharides  Glucose + glucose = maltose  Glucose + galactose = lactose  *lactose intolerance = inability to break down lactose, NOT a milk allergy  Glucose + fructose = sucrose o High Fructose Corn Syrup  50% glucose + 50% fructose = sucrose  Cane and beet sugar  Table sugar, processed foods  HFCS: 45% glucose + 55% fructose  Lquid, made in lab  Helps softer foods stay soft/keeps processed food preserved  Made from corn  Sucrose = less processed than HFCS  Oligosaccharides o 3-10 monosaccharides  Raffinose (gal-glu-fruc)  Stachyose (gal-gal-gluc-fruc)  Found in beans, peas, and whole bran  Sometimes fermented in gut using healthy bacteria, unable to be enzymatically digested  gas  Fibers don’t increase blood sugar  Polysaccharides o Starch  Storage form of carbs in plants  Types (we can digest these)  Amylose o Alpha 1-4 bonds of glucose units o Linear molecule  Amylopectin o Branched alpha 1-6 chain polymer o Also has linear long straight chain (alpha 1-4) o Glycogen  Storage form of carbs in animals  From all glucose  Stored in liver and muscle  Highly branched (looks like amylopectin)  Energy source  Get it when we are starving, high epinephrine, etc.  From glycogenolysis o Fiber  Non-digestible plant polysaccharides  Defined by the USDA  Dietary fiber: found intact/intrinsically in plant (e.g. – oats)  Functional fiber: isolated & extracted, beneficial (e.g. – “double fiber bread”, Metamucil)  Types  Insoluble o Doesn’t dissolve in water o Lower transit time (moves through colon faster) o Increases fecal bulk o Helps constipation o E.g. – celluloses, lignans, some hemicelluloses  Soluble o Dissolves in water o Increased transit time (slower) o E.g. – pectin, gum, some hemicelluloses o Helps diarrhea  Fermented by bacteria in colon  Hydrogen, methane gas, CO2, short chain fatty acids o Short chain F.A.’s  Acetic acid, butyric acid, propionic acid o Functions of short chain F.A.’s  Stimulate water and sodium absorption into mucosa  Provide colonocytes with energy  Enhanced immune function  Increases good bacteria in gut  Decreases atrophy of gut  Decreases cholesterol  Excreted as fecal matter  Carries bile with it (soluble fiber does more than insoluble)  Sources:  Fruits, vegetables, and whole grains  DRI: o Men, ages 19-50: 38 g o Men, older than 51: 30 g o Women, ages 19-50: 25 g o Women, older than 51: 21 g  Digestion of Carbs o Begins in mouth  Salivary glandsalivary amylase  Digest alpha 1-4 bonds  Amylose digestion  Can totally digest it in mouth via amylase  Branched starches  Only breaks alpha 1-4 linkages, not the alpha 1-6 bonds  Action of salivary amylase is incomplete  Alpha 1-6 bonds  Time spent in mouth can determine how much is digested o Stomach  HCl inactivates salivary amylase  Does not digest carbs that much  Mostly holds fod o Small intestine  Pancreatic secretions  Bicarbonate – neutralizes chime  Pancreatic amylase – breaks only alpha 1-4 bonds  Brush border enzymes  Sucrase – breaks down sucrose  Lactase – breaks down lactose  Maltase – breaks down maltose  Absorption & Transport o Location  Small intestine o Mechanisms of transport  Passive diffusion  No energy needed  Limited by concentration gradient  Small molecules and solutes  Facilitated diffusion  Needs a carrier protein o Integral membrane protein o Functions as a transporter  Rate determined by: o Concentration gradient o Amount of carriers (“doors”) available o Rapidity of solute/carrier interaction o Rapidity of conformation change of carrier  Active transport  Needs a carrier protein  Requires energy in form of ATP  Pumps against concentration gradient  E.g. – Na+K+ pump o Carb Absorption  Glucose  Sodium dependent  Active transport  Transporter: SGLT1  To maintain Na+ gradient, Na+ must be pumped out of the cell (K+ comes into cell)  Glucose enters hepatic portal system enterocytecapillariesportal systemliver  Galactose  Same as glucose  Can be converted to glucose to meet needs of enterocyte  Fructose  Facilitated diffusion  GLUT5  Transported to liver  Glucose Transporters  GLUT1 – erthyocytes, placenta  GLUT2 – movement across basolateral membrane (enterocytes), fructose transport at liver  GLUT3 - brain  GLUT4 – muscle, adipocytes  GLUT5 – fructose (small intestine)  GLUT6 – spleen, brain  GLUT7 - unknown  GLUT9,10 - liver  SGLT1 – uptake of glucose/galactose at lumen  *transporters that are insulin stimulated: GLUT2, GLUT4, GLUT5, SGLT1 o Transport  Portal circulation (liver)  Facilitated diffusion o Fructose o Galactose o Glucose  At typical intakes, little to no fructose or galactose in peripheral blood  Glucose not taken up by liver: o Facilitated, insulin dependent  Skeletal muscle, adipose tissue o Facilitated, insulin independent  Kidney, brain  Metabolic Pathways of Carbohydrates o Glycolysis  Purpose: oxidation of glucose, energy production  Location: cytosol  Types (2):  Anaerobic (no oxygen): glucosepyruvatelactate  Aerobic (oxygen): glucosepyruvateacetyl CoA  Liver can take up extra glucose (glycogen)  Muscle has to have a concentration gradient (if more glucose in cell than outside, then it stops taking anymore in) o Glucokinase  Functions in liver and pancreas  Upregulated by insulin  Liver doesn’t remove large quantities of glucose from blood unless glucose levels are high o Hexokinase  Functions in muscle, adipose tissue, and brain  Downregulated by G6P  Max. enzyme activity at normal blood glucose levels o Anaerobic Glycolysis  Energy production: o ATP glucoseG6P = -1 ATP F6PF-1,6-BP = -1 ATP 1,3-BPG3PPG = +2 ATP PEPPyruvate = +2 ATP o NADH G3P1,3-BPG = +2NADH PyruvateLactate = -2 NADH o Net energy production = 2 ATP o Aerobic Glycolysis  Energy Production o ATP (same as above) = +2 ATP o NADH G3P1,3-BPG = +2 NADH (x3=6 ATP) Pyruvateacetyl CoA = +2 NADH (x3=6 ATP) o Net energy production = 14 ATP o Krebs Cycle  TCA cycle, citric acid cycle, etc.  Amphibolic pathway  CHO, fats, & proteins can all enter and be completely oxidized into CO2, H2O, and energy  Provides precursors for synthesis pathways  Location: mitochondrial matrix  Products:  Co2 – exhaled by lungs  H2O  Energy o GTP = 1 ATP o FADH = 2 ATP (in reality b/c of uncoupling: 1.5) o NADH = 3 ATP (in reality, b/c of uncoupling: 2.5)  Energy  Beginning w/ Acetyl CoA 3 NADH x 3 = 9 ATP 1 FADH x 2 = 2 ATP 1 GTP = 1 ATP TOTAL: 12 ATP  Beginning w/ Pyruvate 4 NADH x 3 = 12 ATP 1 FADH x 2 = 2 ATP 1 GTP = 1 ATP TOTAL: 15 ATP Total energy production from 1 molecule of glucose under aerobic conditions = 38 ATP (max yield)  The Shuttle Systems  Malate-Aspartate Shuttle o Moves NADH into mitochondria (ETC) o In liver, kidneys, & heart  Glycerol-3-Phosphate Shuttle o NADHFADH o Enters at complex 3 of ETC o FADH yields 2 ATP o In muscle and brain o Electron Transport Chain  Purpose: production of mitochondrial ATP; changes FADH & NADH to ATP  Location: cristae of mitochondria  Oxidative Phosphorylation  Oxidation: loss of electrons or hydrogens  Phosphorylation: addition of phosphorous  Uncoupling: a pathway starts but doesn’t finish and halts action of ATP synthesis  Proton Gradient  Diffuse from higher to lower concentration  Must maintain a higher concentration of protons in outer mitochondrial space (“intermembrane space”) vs. inner mitochondrial space (“mitochondrial matrix”)  Maintain gradientuse proton pumps (pump from high to low conc.)  Proton Pumps  3 of them: o Complex 1: NADH dehydrogenase o Complex 3: cytochrome B-C o Complex 4: cytochrome oxidase  Complexes which removed electrons from coenzymes located in the inner mitochondrial space and/or pump protons into outer mitochondrial space  NADH hits all 3 complexeseach one makes 3 ATP  FADH starts at complex 3 each one makes 2 ATP  Electron Transporters  Transport electrons b/t complexes in ETC (electron transport chain) o Ubiquinone: transports electrons b/t complex 1 and 3 o Cytochrome C: transports electrons b/t complexes 3 and 4  ATP Synthase (actual “pumping”)  Transports protons across inner mitochondrial membrane into matrix for phosphorylation (ADP + Pi ATP)  Uses B vitamins  Thyroid Hormone o Associated w/ uncoupling proteins o Uncouple oxidation-phosphorylation reactions o Hyperthyroidism:  Increased production of uncoupling proteins  Inefficient ETC – heat loss (burn more glucose to make same amount of energy)  Higher BMR, weight loss, warmer  Lose concentration gradient  Can grow out of it o Hypothyroidism  Can result in a goiter/enlarged thyroid gland  “perfect system” – less glucose to make energy, rest of glucose stored as fat  Low production of uncoupling proteins (*everyone has some uncoupling proteins and some that don’t)  Lower BMR, weight gain, cold, lethargic, deeper voice  Usually around for life  Gluconeogenesis o Synthesis of glucose from non-CHO sources (EXCEPT fat)  Pyruvate  Krebs cycle intermediates  Amino acids  Lactate o Not just the reverse of glycolysis  Acetyl CoA can go back to pyruvate  Pyruvate cannot go back to PEP o Why?  Makes glucose when CHO isn’t available  Hypoglycemia can cause brain dysfunction, coma and death  Clears lactate produced by muscle via Cori Cycle o Liver is the only tissue that can use a phosphate to make a glucose to put back in the bloodstream (usually once a cell is phosphorylated, it stays in the cell)  Glycogenesis o Glucoseglycogen (storage) o Liver – main site of glycogen metabolism and storage o Induced by: high glucose, G6P, & insulin o Never making and breaking glycogen at the same time o Can only store finite amounts in liver o Extra glucoselipolysisstored as fats  Glycogenolysis o Glycogenglucose o Liver-main site of glycogen metabolism and storage o Induced by low glucose, glucagon, epinephrine (need energy for ‘fight or flight’ response)  Epi: more energy neededmore glucose; elevated blood glucoseafter stressful events  HMP Shunt: o “hexose monophosphate shunt”/”pentose phosphate pathway” o Products  Pentose phosphates – used for synthesis of nucleic acids  NADPH (NOT used for energy) – synthesis of fatty acids & cholesterol  Cori Cycle o Intense exercise (lactate producing) o Clears lactate from the muscleback into glucose in muscle (recycles the glucose) o Uses anaerobic glycolysis & gluconeogenesis o Even though the pathway seems inefficient because of the net -4 ATP for the whole body, the muscle is still getting energy so it’s still a good system. o Not all lactate gets sent to liver; some stays in muscle and continues to build up  Regulation of Blood Glucose o Eat a CHO rich meal  Digestion to glucose, fructose, and galactose  Blood glucose increases (when it is in peripheral bloodstream, the pancreas secretes insulin to help glucose get into cell) o Secretion of Insulin  In response to increased blood glucose  Released by beta cells of pancreas  Insulin binds to receptor in cell  GLUT4- allows glucose to enter cell (muscle cells have GLUT4)  Blood glucose levels decrease o Secretion of Glucagon  In response to low blood sugar  Released by alpha cells of pancreas  Stimulates glycogenolysis and gluconeogenesis  We go to glycogenolysis first because it is free and our main storage compartment (“savings account”) for glucose  Integration of CHO cycles (mostly on drawings) o 2 ways to make glucose:  Glycogenolysis (1 choice)  Gluconeogenesis o We rarely use amino acids (protein) for energy; they are used to make neurotransmitters, muscle fibers, bone tissue, etc. (everything else, mostly) o We mainly use carbs and fat for energy o When the body is fed:  Glycogenesis (store glucose in the form of glycogen) o When we need energy:  Glycogenolysis (from glycogen)  Gluconeogenesis (from lactate, amino acids, etc.)  Both above processes then go to glycolysis (aerobic or anaerobic)  Fructose: o Sources:  Table sugar = 50% fructose + 50% glucose  HFCS-42=42% fructose + 53% glucose  HFCS-55= 55% fructose + 42% glucose  Honey=49% fructose + 43% glucose  Apple Juice=59% fructose + 31% glucose o “non-processed foods vs. low fructose”  Agave nectar has more fructose than glucose but it non- processed. Whether or not you choose to eat high fructose foods or non-processed foods depends on your diet goals. o HFCS can make food softer (e.g. – cookies, cakes) and can also increase shelf life. o Absorption  GLUT5  Enterocyte  Converted to glucose  Conversion is dose dependent  GLUT2  Leaves the cell just like glucose and galactose o Portal Bloodstream  At low levels, all fructose is taken up by liver  At high levels, it’s found in peripheral bloodstream o Liver  Metabolism of fructose  Fructokinase  Skips rate-limiting enzyme PFK o De novo fatty acid synthesis (pretty much, if there’s extra fructose, it will be turned into fat) o Non-alcoholic fatty liver disease o Triglycerides in peripheral bloodstreamincreased LDLs  Excess fructose travels in peripheral bloodstream o Peripheral Bloodstream  Fructose doesn’t stimulate insulin  Insulin o Low blood glucose o Promotes carb storage o Promotes satiety o “Is fructose really the enemy?”  Does HFCS cause disregulation of blood glucose? – can be due to a multitude of factors put together  High insulin levels? = insulin resistance? – most likely  Build up of TGs in liver, fatty liver? – yes  Increased TGs in bloodstream? – yes  Increased VLDL hence LDL in bloodstream? – yes  Lack of satiety? – maybe o The real enemy is…  The amount of carbs total coming into the body, not whether or not it’s specifically glucose or fructose (they’re both sugar). o “Is HFCS worse than sucrose?”  Amount per day has increased over the years (24 g/d in 1930’s  73 g/d in present)  1975-1985 HFCS started being used in processed foods (less expensive, more corn available)  Total calorie consumption has increased  More processed foods than ever before  HFCS diet vs. sucrose diet (research – Princeton):  Rats that ate more HFCS ate less but gained more weight, especially around abdominal region  Other research:  No differences between HFCS and sucrose Carbohydrates – Pathways /Charts HUN3224 Diabetes – HUN3224  Blood Glucose Values o Normal Fasting – 60-100 mg/dL o Elevated – 100-125 mg/dL o Hyperglycemia - >126 mg/dL o Hypoglycemia - <50 mg/dL o HbA1C – 7%  Glycated hemoglobin  Good at determining/examining long-term control of blood glucose levels  Types of Diabetes o Diabetes Mellitus Type 1  Causes  Autoimmune or viral damage to beta cells  Reduced insulin production o Glucose cannot move into cells o Glucose remains in blood  Usually diagnosed in children and teens  Uncontrolled diabetes o Still has better control than type 2 and there are usually fewer complications than type 2  Symptoms  Weight loss (cells use fat instead of glucoseketosisketones provide less energy than CHOburn more fat)  Increased urination  Ketosis (using fat)  Long-term complications  Kidney disease, blindness, poor circulation, CVD, impaired nerve conduction  Treatment:  Insulin (2 peptides together, can be synthetic) o Insulin pumps o Injections – medications need to be refrigerated  Diet o Carb controlled (know amount of carbs) o Amount of food o Time of food/know how rapid the insulin is  Usually the whole family is involved and educated o One reason type 1 diabetes is so well controlled (more controlled than type 2)  Goal: stable blood glucose levels o DM (“Diabetes Mellitus”) Type 2  Causes/Complications o Begins as insulin resistance  diabetes o Obesity, diet, genetics, inactivity o Correlation between adipose tissue amounts and diabetes o Genetics can affect it as well (nature vs. nurture conversation)  Symptoms/Long-Term Complications o Similar to type 1 o Pancreatic insufficiency – can stop making insulin so they need insulin and resistance medications  Treatment o Weight loss o Exercise o Diet o Pharmaceuticals  Metformin/Glucophage – prevents gluconeogenesis, glycogenolysis  Glipizide/Glucotrol – tells pancreas to make more insulin  Insulin o Needs to be diet-controlled while taking meds  Medications only work at certain levels  Not “fix alls” o Education  Type 2 diabetes education – expensive, some people don’t know about it  Type 2 diabetics usually aren’t as educated as type 1 diabetes  Symptoms of Uncontrolled Diabetes o High blood glucose levels associated with dyslipidemia o Dyslipidemiamicrovascular diseasesdecreased blood flowhigh risk of infection, longer to heal numbness o Neuropathy  Decreased blood flow  Decreased nerve signaling, lose sensitivity  Lose feeling in hands, feet, etc.  Sores, bruises, cuts, etc.  Infection, gangrene, amputation  #1 cause of non-trauma amputations is type 2 diabetes (>60%)  Risk is 10x higher in diabetics for amputations  GI Tract  Intermittent diarrhea, constipation  Thickening, cracking, bleeding  can lead to infection  Gangrene spreads through limbs, can be quick (days) o Retinopathy  New capillaries form to compensate for decreased blood flow and increased oxygen  New capillaries are fragile  Prone to bleeding  Microaneurysms  Lesions  Undergo fibrosis  Macular edema – fluid leaks into eye  Leading cause of new blindness  Usually in type 2 diabetics  From high levels of glucose for a long time  Short term: blurry vision o Nephropathy  Decreased kidney functioning  Can cause renal disease  Uncontrolled diabetes – leading cause of kidney failure  Kidney failure  Dialysis o When kidney function decreases to 10-15% at normal o 3-4 hours, 3-4 times a week (time-consuming process)  Types of Dialysis o Hemodialysis  AV fistula – implanted, move it over a period of time because scar tissue builds up  Graft  Catheter o Peritoneal  Passive diffusion of toxins through peritoneum (abdomen – peritoneal cavity)  “wet abdomen”  Diet – Diabetes & Dialysis o Diabetes  Continue with carb control o Dialysis  Fluid  They may not urinate anymore  Avoid foods with high water content: veggies, soups, fruits, ice cream, jello, drinks  Potassium (potatoes, bananas)  Phosphorous – take phosphorous binders, patient can feel itchy  Protein – kidney gets rid of extra nitrogen but the kidneys are not working properly  Sodium o Gestational Diabetes (onset w/ pregnancy)  Abnormal glucose tolerance during pregnancy  Excess weight gain during pregnancy and obese women pre-pregnancy have high incidence of gestational diabetes  Some women with it will develop type 2 diabetes post- pregnancy, especially if they’re overweight  Does not seem to be correlated with type 1  It increases risk of:  Macrosomia (big babies) o Extra nutrients pass from mom to baby o Baby grows as big as it wants  NICU stays o Problems with breathing, developmental issues, prematurity  Hypoglycemia after birth o Glucose can pass from the mom to baby but NOT insulin o Baby makes own insulin  hyperinsulinemia o After the umbilical cord is cut, the insulin is still high even though there’s no more glucose (only glucose supply is cut off)  hypoglycemia o Hypoglycemia  Can occur in diabetics (more common) and non-diabetics  Considered more dangerous than type 1 and 2  Symptoms:  irritability, dizziness, headache, shakiness, confusion, seizures, coma, death, unconsciousness, sweating  Prevention:  Match insulin and medications with meals  If you’re doing more activity than usual, have a snack first  Don’t drink excessively and don’t drink on an empty stomach  Treatment:  15/15 rule: check blood glucose, eat 15 g of carbs, wait 15 minutes  2-3 glucose tablets  ½ cup fruit juice or soda, not milk (mostly fats and proteins)  5-6 pieces of hard candy/pure sugar (e.g. – icing)


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