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Exercise Is Medicine > T2DM > Flashcards

T2DM Flashcards

1
Q

pancreas
1. function
2. comp
3. developing exogenous insulin

A
  1. endocrine gland func to reg blood glucose levels, exocrine gland function to secrete pancreatic juice into duodenum for digestion
  2. endocrine portion of the pancreas is comp islets of Langerhans (1%) and exocrine acini cells (99%)
  3. insulin purification process dev by Canadain scientists Frederick Banting and Charles Best
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2
Q

composition of islets of Langerhans

A
  1. beta cells produce insulin to lower BG by increasing glucose uptake, marcomolecule synthesis, and inhibition of TG breakdown
  2. alpha cells produce glucagon to raise BG via liver glycogenolysis and gluconeogenesis
  3. delta cells produce somatostatin
  4. F cell produce pancreatic polypeptide
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3
Q

diabetes overview

A
  1. diabetes is a group of metabolic disease characterized by hyperglycemia
  2. type I is the inability to regulate BG due to deficient insulin secretion from beta cells
  3. type II is the inability to reg BG due to lack of insulin sensitivity in normally insulin-sensitive tissues
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4
Q

glucose regulation
1. insulin
2. exercise and glucose uptake

A
  1. insulin increases the speed of glucose uptake from blood into cells, with insulin res lose the ability stim translocation of GLUT4 transporter (how majority glucose gets transported), still able to transport glucose through GLUT1 but much slower, BG rises
  2. exercise can induce GLUT4 translocation, allowing skeletal muscle to act as a glucose sink
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5
Q

T1DM therapeutic intervention
1. monitoring glucose
2. exogenous insulin
3. insulin delivery

A
  1. BG measured throughout day to keep BG in noroglycemic range (70-180 mg/dL)
  2. since beta cells cannot produce insulin, deliver exogenous insulin; 4 types: rapid-acting controls spike, short-acting is regular insulin peaking at 2-3 hr, intermediate-acting allows peak in 4-12 hrs, and long-acting with no peaks working over 24 hr
  3. insulin injected into subQ fat with needle, modern ver use BG monitor which detects increase in glucose and signal tube under skin to release of rapid-acting insulin from pump
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6
Q

diabetes epidemiology
1. overview
2. T2DM risk factors
3. T2DM epidemiology

A
  1. type I and type II affect 15% if pop; with 5-10% T1DM and 90% T2DM; diabetics x3 more likely to be hospitalized with CVD
  2. age due to dysreg of cellular functions, POC, family history of T2DM or genetic factors; symptoms of MetS, obesity, poor lifestyle choices
  3. prevalence of T2DM is increasing in the world but incidence (new cases) has been decreasing since 2010
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7
Q

T2DM clinical manifestations
1. non-specific clinical manifestation
2. long term manifestation
3. mechanisms and pathogenesis

A
  1. have symptoms of MetS such as overweight, dyslipidemia, hyperinsulinemia, and high BP; fatigue, classical symptoms of polyuria, polydispsia, and polyphagia (too much urination, drinking, and eating); unexplain weight loss due to poor metabolic cycling (glucose cannot be uptaken, fats and proteins are broken down to provide fuel); recurrent infections (high BG breakdown neural and vascular tissue) and poor wound healing (breeding ground for organisms consuming glucose)
  2. microvascular and macrovascular complications and steatohepatitis
  3. due to B cell dysfunction, insulin res, whole body chronic inflammation
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8
Q

insulin resistance and altered beta cell physiology

A

dysregulation of BG feedback sys begins when too much glucose is in body for long time, beta cells become stressed/overactive and hypertrophy to compensate for high BG; beta cells fail, ratio of alpha to beta cells increase and beta cell sensitivity decrease, dev glucolipotoxicity and insulin res; beta cells then undergo differentiation and death, decreasing beta cell mass by 30-40% leading to diabetes

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9
Q

genetic vs. lifestyle factors of T2DM

A
  1. mother > father T2DM risks; SNP in adipocyte TCF7L2 (Wnt signalling pathway) increase risk by 10-20% and in vitro or in vivo inactivation of TCF7L2 increase adipocyte hypertrophy and insulin res; however 55% of people w/o T2DM have risk allele so influence of genetics is less than influence of lifestyle
  2. obesity is the single most important predictor; 90% of cases are preventable by following healthy habits
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10
Q

multiorgan cause of chronic hyperglycemia: adipose tissue

A
  1. adipose tissue produce leptin and adiponectin, obesity increases leptin decreases leptin sensitivity, gen less satiety
  2. decreases adiponectin decrease BG reg high food intake increase BG, increases inflammation and decrease insulin sensitivity
  3. adiposity assoc with high amounts of serum (bound to albumin) FFAs, inflammatory cytokine TNF alpha, and decrease insulin receptor density, all of which increase inflammation and insulin sensitivity
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11
Q

multiorgan cause of chronic hyperglycemia: pancreas

A

altered inuslin and glucagon signaling, decrease amylin (beta cell hormone secreted with insulin to increase saitety and decrease glucagon release)

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12
Q

multiorgan cause of chronic hyperglycemia: GI tract

A

decrease ghrelin (reg E balance and food intake) produced in islet cells for insulin res and decrease fasting insulin; decreased beta cell sensitivity to GLP1 and GIP (big moderating factor of insulin secretion)

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13
Q

multiorgan cause of chronic hyperglycemia: kidneys
3. brain

A

reabsorb glucose from urine using sodium glucose cotransporter 2, high glucose saturates SGLT2 and left over glucose goes into urine but high uptake at kidneys worsens hyperglycemia

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14
Q

multiorgan cause of chronic hyperglycemia: brain

A

manages satiety, insulin, and glucose detection, brain uses 20% of body glucose at rest; high glucose cause neuroinflammation, GLUT1 and GLUT3 have impact on neuro condition such as Alzheimers

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15
Q

insulin signalling in adipose cells
1. overview
2. inflammation in dysfunctional adipose cells
3. dev of insulin res

A
  1. insulin bind to insulin receptor and IRS trigger casade, activating PI3Kp (p=phos) and PDKp, PDKp activates PKC delta and AKT, PKC delta signals GLUT4 movement and AKT inhibit AS160 (AS160 inhibits translocation) to induce translocation of GLUT4 and FAT CD36 to transport GLU and FFA into cell respectivity, FFA and GLU then be stored as TG in lipid droplet in cell; when need fuel, can breakdown TG into FFA and transport into blood for use
  2. functional adipocytes have high amounts of O2, able to produce lots of ATP; dysfunctional addipocyte stores high amt of TG, hypertrophied, less O2 per cell, decrease ATP production leading to cell death and secrete TNF alphha which recruites macrophages to release more inflammatory cytokines
  3. TNF alpha inhibit IRS, blocking downstream cascade at the start; cannot uptake FFA to be stored and move FFA to blood thus high serum FFA
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16
Q
  1. insulin signalling in skeletal muscle on metabolism
  2. adiposity on dev of insulin res
A
  1. insulin bind to receptor, IRS trigger signalling cascade to bring in glucose and FFA; conversion of FFA produce ceramides and DAG, DAG converted to TAG (triacylglycerol) for fuel; GLU either converted to glycogen or metabolize by mitocondria
  2. bring in high amount of circ FFA, accumulating high amounts of ceramides and DAG, DAG inhibit IRS and thus insulin signalling and ceramides dysregulate AKT and PKB for GLUT4 translocation, less GLU uptake; mitocondria working harder to use up extra E, breakdown due to excessive use due to gen of high amounts of reactive oxidative species
17
Q

assessing and diagnosising T2DM
1. parameter
2. short and long term post prandic response

A
  1. high HbA1c is glycated (chem linked) hgb, high fasting plasma glucose (not able to take in glucose as well due to insulin res), 2 hr plasma OGTT (measure ability to use glucose over 2 hours, homeostatic model assessment for insulin res (HOMA-IR) comp fasted GLU to insulin
  2. after OGTT area under the curve (decreasing BG curve) should return to normal after 120 mins, in the long term measure HbA1c at 90 days to see how much hgb is glycated; glycated hgb cause dmg since glucose crystals in blood physically scratch body, increases inflammation
18
Q

metformin for T2DM

A

most commonly prescribed med to decrease hepatic GLU production to decrease HbA1c by decreasing mitochondrial oxidative phosphorylation, decrease liver production of glucose via AMPK activation, and induce lactic acidosis to decrease gluconeogenesis; decrease ability to use new glucose and force body to use existing GLU

19
Q

glucagonlike pepetide 1 agonist

A
  1. GLP1 responds to elevated BG and induces insulin secretion, is broken down by DDP4
  2. Ozempic chem identical to GLP1 but is res to DDP4 thus able to mimic the effects of GLP1 to increase insulin secretion, decrease glucagon secretion, and decrease gastric emptying
20
Q

exercise molecular mechanisms on T2DM

A

exercise increase Ca2+, increase calmodulin which causes cascade of events inducing exercise induced GLUT4 translocation and increase AMPK which inhibits AS160 allowing GLUT4 translocation

21
Q

T2DM management types
1. diet
2. exercise
3. medications
4. lifestyle vs. medication

A
  1. prevents large spikes in glucose
  2. facilitate glucose uptake and promote weight loss (less adiposity less inflammation)
  3. increase insulin sensitivity, slow digestion, block renal GLU reabsorption, increase insulin
  4. longitudinal study over 5 years, lifestyle intervention has greater decrease in risk of T2DM over metformin, decrease metformin with increase E expenditure per week
22
Q

T2DM management exercise
1. acute changes
2. chronic changes

A
  1. stim increase contraction-induced GLUT4 translocation and increases insulin sensitivity for 24-72 hours to manage BG
  2. decrease adiposity by decreasing serum FFA and decrease inflammation by using TG stores, produce less TNF alpha, less use of mitochondria to use up fuel, less reactive O2 species, mitochondria can stay healthy; increase mitochondria and mitochondria enzymes increases efficiency
23
Q

END vs. HIIT on T2DM

A
  1. trad END is well documented in preventing and treating T2DM, usually at lower intensity, better tolerated
  2. HIIT can provide great effects for shorter time but may not be tolerated by all, may need start very light and build up
  3. both END and HIIT improve VO2max and HbA1c but HIIT shows greater improvement; other variables such as FPG, fasting insulin, insulin res, BP, blood lipid, etc., more research needed
24
Q

T2DM, exercise, and comorbidities risk

A

T2D assoc with many comorbidities such as CV conditions, strokes, neuropathy (increased fall risk due to decreased neural control and feedback)

25
Q

creating exercise programming for T2DM
1. ACSM and CSEP recommendations
2. exercise timing

A
  1. primary focus on decreasing adiposity, some exercise is better than none but recommend doing CV, strength, muscular END, and flexibility/balance throughout the week
  2. reduce glucose spikes by exercising before meal to increase GLUT4 translocation before, longer durations of aerobic are best for long term glucose management throughout the day but resistance is also effective since it greatly increases Ca2+ to stim GLUT4 and increased muscle mass allows for greater ability to uptake glucose and decrease HbA1c; best performs bouts less than 72 hours apart to maintain level of GLUT4 translocation
26
Q

considerations of exercise and T2DM

A
  1. SNS activity can lead to hyperglycemia but stimuli typically not strong enough, too muscle glucose uptake leads to hypoglycemia but hard to exercise long enough for this to occur, usually more related to poorly timed insulin dosage
  2. check that glucose is in normal range and no recent insulin intake or other medications that can affect exercise before starting

Exercise Is Medicine (8 decks)

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