3/27 LIPIDS, CARBS MCBRIDE

• Maintaining homeostasis requires metabolic regulation that coordinates the use of nutrient pools
• Homeostasis adjusts production and consumption rates to maintain physiological levels while also meeting essential demands.
• homeostatic mechanisms

  • adjust rates to achieve production=consumption

  function: to maintain physiological concentration required for life
• caloric homeostasis

  • means of regulating energy stores
  • ABILITY TO MAINTAIN ADEQUATE, but not excessive energy stores
• excess energy fuels (aka nutrients) must be stored

  • if fuels are consumed in excess of energy needs, fuels are stored
  • excess energy are CONVERTED to TRIACYLGLYCEROLS --stored in adipocytes
• what fuel is consumed?

  dietary protein, fats, carbs
• energy stored as triacylglycerols
• fuel EXPENDED

  • AA, FATTY ACIDS, MONOSACCHARIDES, OXIDIZED IN TCA CYCLE
• excessive triacylglycerol storage has adverse health effects

  • excess storage of triacylglycerols when food is scarce.. that way, when no food , u can still make energy and maintain energy supply
  • continued energy storage (if u store too much energy)
  • accumulation of triacylglercols
  • enlarged adipocytes
  • body weight gain
• health consequences of increased body fat

  • storing too much, can lead to stroke, type 2 diabetes, cancer, hypertension, liver, sleep apnea
• how is energy balance controlled?

  by behavioral and biochemical factors . find a balance
• Behavioral factors: diet/nutrient consumption, exercise
• Biochemical factors: Short-term and long-term signals, resting metabolic rate, hormones
• energy intake

  • how we take in energy (can be thought of as calories)
  • via food, alcohol consumption
• energy expenditure

  • basal metabolism
  • thermogenesis
  • physical activity
  • # of calories burned/broken down
• two types of signals in gastrointestinal tract

  • beta cells of pancreas, fat cells/adipocytes
  • short term signals --> active during meal
  • long term signals --> overall energy status of body
• short term and long term signals target...

  • brain's arcuate nucleus aka a group of neurons in the hypothalamus
• what is secreted from small intestine signal distal organs like brain and pancreas?

  small peptide hormones
• short term signals (when eating ex.)

  • feelings of satiety( full) from gut to brain
  • reduce urge to eat , stop eating
• CCK, GLP-1 : Cholecystokinin (CCK) and glucagon-like peptide 1 (GLP-1)

  • small peptide hormones secreted into the blood by cells of small intestine after a meal
  • bind to their G Protein coupled receptors in peripheral neurons, relay satiety signals
• CCK stimulates secretion of pancreatic enzymes and bile salts from gallbladder.
• SIGNALS:

  • PANCREAS --> increased insulin secretion, insulin biosynthesis
  • BRAIN --> increased satiety , decreased food intake, decreased body weight
• GLP-1 enhances glucose induced insulin secretion and inhibits glucagon secretion.

  
  

  • insulin, GLP1 secretion promotes energy storage
  • increase insulin secretion
  • increase glycogen synthesis and lipogenesis (aka turns glucose into fatty acid)
  • decreases lipolysis
  • glucagon decreases energy storage (bc its using it up)
• GLUCAGON

  • DECREASES energy storage
  • activates lipases to catalyze hydrolysis or triacylglycerols to fatty acids
• GLP-1 agonists

  • new line of med to regulate blood sugar and lipid storage
  • how do they work?
  • mimic GLP-1 hormone
  • trigger insulin release from pancreas
  • decrease glucagon secretion
  • decrease rate of digestion/stomach emptying
  • increasing feelings of being full /satiety ..so that u dont eat
• LEPTIN (makes u skinny)

  • LIKE INSULIN, REGULATES LONG TERM CONTROL OVER CALORIC HOMEOSTASIS
  • signal molecule that communicates the STATUS of triacylglycerol stores
  • suppresses appetite
  • secreted by adipocytes
  • secreted in direct proportion to amount of fat(to even)
  • binding to its receptor increases the sensitivity of muscle and liver to insulin, stimulating beta oxidation of fatty acids, decreases triacylglycerol synthesis.
• insulin

  • signal molecule that communicates the status of glucose in blood
  • secreted by pancreatic beta cells
• Leptin

  • adipokine secreted by adipose tissue in direct relation to fat mass
  • When fat mass increases, leptin inhibits appetite-stimulating peptide (NPY and AgRP) secretion (lack of appetite, to not eat)
  • stimulating the release of appetite-suppressing hormone (MSH).
• fasted-fed cycle

  • physiological condition experienced after an evening meal, throughout the night's fast
  • 3 stages : well fed (postprandial), early fasting (postabsorptive), re-fed state
• glucose homeostasis - constant blood-glucose concentration

  • maintained during the fasted fed cycle by insulin and glucagon
• post absorptive (fasted) state = state that immediately follows the absorption of glucose from previous meal when blood-glucose concentration begins to drop

  • DECREASE in insulin secretion, INCREASE in glucagon
  • BC UR HUNGRY ..
• GLUCAGON

  • stimulates glycogen breakdown (to get the stored glucose)
  • inhibits glycogen synthesis (inhibits STORED GLYCOGEN BC U SHOULDNT BE STORING IT WHEN U NEED IT )
  • inhibits fatty acid synthesis (Glucagon inhibits fatty acid synthesisto prioritize the use of existing energy stores for raising blood sugar levels quickly)
  • stimulates gluconeogenic state in liver (gluconeogensis to make more glucose)
  • block glycolysis
  • 1st responder when blood glucose levels drop..
• phosphofructokinase

  • key enzyme in regulation of glycolysis
• fructose 1,6-bisphosphataseatase

  • principal enzyme controlling the rate of gluconeogenesis
• after long fast, u eat, and liver uses glucose to replenish glycogen stores .

  
  

  when fasted- used glycogen stores .

  so now when u have glucose replace it and turn it into glycogen
• fat is processed the same in normal fed state vs re-fed state
• post fast

  • liver doesn't initially absorb glucose from blood
  • liver remains in gluconeogenic mode
  • replenishes stored glycogen
  • then liver processes excess glucose for fatty acid synthesis
• diabetes

  • disease due to disrupted glucose homeostasis resulting from insulin resistance
  • overproduction of glucose by the liver
  • underutilization by other organs
  • excessive urination
• with diabetes, increased glucose elevation and slower clearance after a meal. (hard to get rid of )
• TYPE 1 DIABETES

  • insulin dependent
  • caused by destruction of insulin secreting beta cells of pancreas
  • autoimmune disorder
  • before age 20