Lecture 31: Nutrition Flashcards
Macronutrients
Carbohydrates
Protein
Lipids
Micronutrients
Minerals
Vitamins
Basal metabolic rate
Energy expenditure at rest, warm, awake, several hours after a mean
High in males tan in females
Decreases with age after reaching adulthood
Different in between organs and tissues
Brain is 25% of BMR
Total energy expenditure
Basal metabolic rate + thermic effect of food + physical activity
Protein digestion
- Dietary protein broken down by pepsin into polypeptides and amino acids
- Broken down into oligopeptides and amino acids by pancreatic proteases and peptidases
- Broken down completely to amino acids by intestinal peptidases to be absorbed by small intestine and taken to liver
Carbohydrate digestion
- Starch, lactose, sucrose, cellulose taken in by both and broken into disaccharides by alpha-amylase
- Broken down by pancreatic amylase
- Broken down by sucrase, lactase, maltase and isomaltase
- Absorbed by small intestine and sent to liver (cellulose secreted as feces)
Lipid digestion
- Emulsification by bile salts and digestion by pancreatic lipase (triacylglycerols cannot cross membrane by simple diffusion, not soluble in water, present in big droplets)
- Free fatty acids, glycerols and cholesterol taken up by enterocyte and reesterified into chylomicrons in lymph to be send to blood
Emulsification
Big fat globules are broken into small droplets
Bile acids act as detergents
Increased surface area
More exposure to lipase
Lipolysis
Breakdown of triacylglycerols
Resulting monoacylglycerols are taken up into intestinal cells
Monoacylglycerols
Taken up into intestinal cells
Synthesized into triacylglycerols and secreted in form of chylomicrons
Pancreatic lipase
Digests triacylglycerols into 2-monoacylglycerols releasing 2 fatty acids
Chylomicron metabolism
- Intestinal mucosal cells secrete TG rich chylomicrons
- Enters capillaries
- Degraded by lipoprotein lipase into glycerol (to liver) and fatty acids (to adipose)
- Chylomicron remnants bind to specific receptors on the liver and are endocytosed
VLDL metabolism
- Secreted by liver
- Enters capillaries
- Lipoprotein lipase digests into fatty acid (to adipose) and glycerol (to liver)
- Left is LDL which is sent to extra hepatic tissues and on liver and are endocytosed
Muscle metabolic profile
Takes up fatty acids form adipose, and VLDL/fatty acids/ketone bodies from liver
Sends alanine and lactate to liver
Brain metabolic profile
Takes glucose and ketone bodies from liver
RBC metabolic profile
Take glucose from liver
Send lactate to liver
Heart metabolic profile
Takes glucose/VLDL/fatty acids/ketone bodies from liver
Takes fatty acids from adipose
Adipose tissue metabolic profile
Sends fatty acids to muscle and heart, fatty acids and glycerol to liver
Takes VLDL/fatty acids/glucose from liver
Diabetes mellitus
Chronic disorder of carbohydrate, fat and protein metabolism
Elevation of plasma glucose levels (hyperglycaemia) because of defect or deficiency of insulin secretion from pancreas
Increased thirst, unexplained weight loss, increased urination
Metabolism resembles the post-absorptive or fasting state with low insulin
DM Type 1
Destruction of pancreatic beta cells (often autoimmune response)
Complete absence of insulin, increased levels of glucagon even when dietary glucose is present
DM Type 2
Insulin resistance
Insulin is secreted but the cellular response is impaired
Later impaired glucose-stimulated insulin secretion develops as well
Insulin resistance
Signalling interrupted
Fatty acids, inflammatory cytokines and other molecules trigger other signalling cascades that interfere with intracellular insulin cascade from receptor binding
Hyperglycaemia effect of diabetes
Decreased glucose uptake into muscle and adipocytes
Ongoing gluconeogenesis
Glycogen breakdown in liver
Amino acid uptake with diabetes
No insulin so amino acid uptake and protein synthesis are not stimulates: gluconeogenesis precursors
Fatty acid uptake with diabetes
No insulin, high glucagon
Increase hormone sensitive lipase activity
Fatty acids taken in as gluconeogenesis intermediates
Lipoprotein uptake with diabetes
Insulin inhibits VLDL secretion and activated lipoprotein lipase
No insulin causes decrease in clearance of TG-righ lipoprotein, increased VLDL secretion
Characteristics of cancer cells
- Uncontrolled growth
- Growth without attachment
- Growth without external growth factors
- Dedifferentiation