Diabetes: Nutritional Mechanisms, NIM

how much glucose absorbed in intestines per hour?
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Terms in this set (39)
how much glucose absorbed in intestines per hour?
1 gram per kg body weight per hour
where are they mostly absorbed
duodenum, jejunum
what is glucose converted to in the liver? what process needs to happen first to the molecules? where does it go if there is excess
glycogen

phosphorylation

taken to rest of body
how does the body metabolize xylitol and sorbitol
these sugar alcohols are digested slowly
diabetic diet. why?
several small meals throughout day,

large meals cause prolonged increase in blood glucose throughout the day
lactose is composed of?
glucose and galactose
maltose? sucrose?
glucose x2
glucose + sucrose
bruch border enzymes cleave? cannot cleave?
disaccharides into monosaccharides for absorption via active transport/facilitated transport

can't cleave some polysaccs, which is considered then, fiber
which molecules can enter the glycolytic pathway?
fructose, galactose, glucose
where is amylase produced?
saliva and pancreas
where do sugars enter the liver?via portal veinGLUT1 is located on? what does it bind to? what about GLUT 2 GLUT 3 GLUT 5?erythrocytes, endothelial cells, widely expressed, glucoseGLUT 4adipose tissue, skeletal muscle, heart INSULIN sensitive glucose transporter high affinity for glucose in presence of insulin2 pathways in cytosol in muscleglycolytic or pentose phosphate pathwayhigh carb load shunts glucose to which pathway?pentose phosphate pathway -> highly anabolic tissues like liver and adipose tissues, but not active in musclefinal common pathway for oxidation of body's fuelscitric acid cyclelactate, oxaloacetate, amino acids can all take part in which process when glucose runs low?gluconeogenesis20% of all glucose goes to what metabolic process? what does this process do?cori cycle, captures lactate formed in muscle, and converts to back to glucose via gluconeogenesis in the liverglucose-1-phosphate increases in fed state?yes, attached to others by glycogen synthasekey enzyme for glycogen breakdown?glucagonshort term complications of diabetes mellitusketoacidosis, hyperosmolarity, lactic acidosislong term complications of diabetes melitusmicrovascular, macrovascular, neuropathological complicationsdiagnosis of diabetes: fasting plasma random plasma a1c value126 200 6.5 confirm on a later, subsequent testinsulin increases: suppresses:increases uptake of glucose into muscle and adipose tissue, amino acid uptake and protein synthesis, fatty acid synthesis and esterification, glycogen synthesis, glycolysis suppresses: usage of glycogen, fat, muscle proteinsregulation of insulin secretionincreased blood glucose, increased amino acids, increased fatty acids, INCRETIN hormones, acetylcholine suppressed by: leptin, sympathetic nervous system (a2 adrenergic, like norepinephrine)deficiency of which micronutrient impairs activity of insulin receptor tyrosine kinasechromiumchromodulinhelps w independent activation of GLUT 4 just need baseline amount, not a large amount (in hope of increasing insulin sensitivity further)glucagon causes an increase in: and a decrease in:increase breakdown of glycogen, lipolysis, gluconeogenesis, ketogenesis decreases: synthesis of glycolytic enzymes, rate of glycolysis, glycogen synthesiswhat stimulates glucagon? what represses it?low blood glucose, increased AAs, a2 receptor repressed by hyperglycemia, increased fatty acids in circulation and somatostatineffect of epinephrine and cortisol?epinephrine (from adrenal medulla) increases glycogen breakdown, gluconeogenesis from lactate and amino acids, mobilization of fat via hormone sensitive lipase cortisol augments epinephrine and glucagoninsulin regulates ____ state via _____ enzyme, glucagon regulates _____ state via ____ enzyme.fed state, glycogen synthase (via dephosphorylation) fasting state, glycogen phosphorylase (via phosphorylation)risk criteria for obesityBMI >25 1st degree relative w diabetes delivery of baby >9lbs impaired glucose tolerance/elevated fasting glucose history of gestational diabetes AA, hispanic, native am, asian american, pacific islander Hypertension (140/90) HDL < 35) or TG > 250mg/dL physically inactivefirst step in pathogenesis of obesity induced diabetes mellitus- visceral fat releases fatty acids, which promotes gluconeogenesis and interferes with insulin signaling - causes hyperglycemia and insulin resistance -> produce more insulin - high insulin -> promotes further weight gain - pancreas beta cell burn out -> T2DMgestational diabetes mellitusmaterial over nutrition -> excessive fetal growth or restricted fetal growth (impaired placental development)when should you screen for gestational diabetes?initial visit, again t 24-28 weeks to assess for moderate risk individualseffect of regular exerciseserum lipid profiles, cardiovascular health, makes childbirth easier (oxidation of free fatty acids in muscle aids weight loss and improves lipid profiles) - stimulates increase in hepatic glucose production, increase in adipose tissue lipolysis - increased glucose uptake, lowers blood glucose, increase glucagon secretion, increase release of catecholaminesbest therapy for gestational diabetes?insulin therapy, along w meal plans to stabilize blood glucose lowering carb intake to < 45% total caloric intakecomplete dietary history would include:- dietary fat, fruit, vegetable consumptionwhat kind of questions should you ask patients during interview? what do you want to avoid?open ended, non judgmental, at their level of understanding instead of using medical terminology - want to avoid them giving answers that are given because its what they think you want to hear (leading question), or because they want to hide something from you (accusatory question)