Obesity & Skeletal Muscle (Quiz #4)

obesity trends US

40% adults obese

costly, leads to chronic illness

non-Hispanics, Blacks, less educated, more affected

what is BMI

body mass index:

- developed by european white men

- standard tool used to identify health risks

- limited by ability to distinguish between muscle and fat mass (especially elderly)

- consistent positive relationship w/ increased risk for disease and mortality rate

white fat

major site of triglyceride storage, and lipolysis (weight gain)

brown fat

contains UCP1 and produces heat, especially in newborns (helps to burn calories)

visceral fat

surrounds organs, linked to cardiovascular diseases and type 2 diabetes

subcutaneous fat

stored under sking, generally less harmful metabolically

when do adipocytes primarily increase?

adolescence, childhood (puberty)

later in life they level off and become stable

what happens to adipocytes when you lose weight?

size: decreases (leaner = smaller adipocytes, less fat stored)

number: no change!!

how does liposuction affect adipocytes?

removes fat cells, but remaining cells may regrow or increase

cause of obesity: medical

some drugs may cause you to retain fluids: steroids, beta-blockers (insulin), anti-depressants

cause of obesity: genetic

susceptibility may be inherited leading to increased risk

cause of obesity: nutritional

increased calorie consumption, ultra-processed foods, high sugar food and drink increases saturated fats

cause of obesity: endocrine/hormonal

decreased sleep, increased stress (cortisol), metabolic syndrome, polycystic ovarian syndrome (women)

cause of obesity: activity-related

lack of physical activity

gut-brain axis

2-way signaling network between the gastrointestinal tract and the brain

hunger hormone: ghrelin

hormone released during fasting, from the stomach, that stimulates hunger. (from pancreas is glucagon)

hunger hormone: leptin

hormone released from adipose tissue that helps suppress appetite

- if mutation in leptin/leptin receptors, may overeat (rare)

hunger hormone: PYY and CKK

2 gut hormones released from GI tract after eating that help reduce apetite:

- PYY = peptide yy, signals fullness "satiety". decreases obesity, increases anorexia

- CKK = cholecystokinin, peptides that help pancreas secrete digestive enzymes and bile

obesity prevention: nutrition

increase nutrition: high fiber, lower fat, lower ultra processed food

obesity prevention: activity

increase activity: cardiovascular, strength training

obesity prevention: sleep

getting enough sleep and mental health support is important in staying healthy

obesity prevention: meds

GLP-1: feel full from less food (agonist)

obesity prevention: surgery

plastic surgery, lipo-surgery

obesity complications

- cardiovascular disease, type 2

- metabolic syndrome: insulin resistance, impaired glucose tolerance

- chronic kidney disease

- end stage organ disease

diabetes

any disorder that increases urine discharge:

- mellitus = high blood sugar (type 1/type 2)

- insipidus = water imbalance, excessive thirst, not enough ADH

type 1 diabetes

insulin dependent diabetes mellitus

- autoimmune, B-cells attacked (lost) so blood sugar high

- symptoms: over 20 years, polys, fatigue, excessive thirst&urine production

- associated with weight LOSS, neuropathy, retinopathy, heart disease risk

- decreased insulin —> treated with insulin injections

type 2 diabetes

insulin independent (preventable)

- down regulation of insulin receptors (resistance)

- symptoms: over 40 years, polys, ulcers, vision loss, frequent infection

- normal or increased insulin

- associated with weight GAIN, neuropathy, retinopathy, heart disease risk

- diet, exercise, sulfonylureas (stimulate insulin secretion), GLP-1 (weighloss, agonist), metformin (inhibits hepatic gluconeogenesis = less glucose)

polyuria

increased urine

polydipsia

increased thirst

polyphagia

excessive eating/feeding

hyperglycemia

high blood sugar

- common in type 1 mellitus

hypoglycemia

low blood sugar, too much insulin

- insulin shock can cause coma and death

- common in type 2 after high carb meal

sulfonylureas

stimulates insulin secretion by blocking ATP gated K+ channels

- stimulus = increased blood glucose

- ATP closes K+ channels which depolarizes cell causing Ca2+ channels to open

- Ca2+ comes into cell allowing insulin vesicles to exocytose out into blood

metformin

Inhibits hepatic gluconeogenesis

- reduce glucose production in the liver

- increase insulin receptors in muscle (up-regulation)

- delay absorption of glucose in the intestine

skeletal muscle

attach to bones, striated, voluntary movement, moves body, one cell = fiber

cardiac muscle

heart, striated, involuntary, pumps blood, contracts via pacemakers

smooth muscle

walls of hollow organs, involuntary, moves fluids, slow contractions

origin of muscle attachment

closer to the main axis, muscle contracts towards origin

insertion of muscle attachment

further/distal, muscle moves this bone towards origin as it contracts

actions around joints are...

antagonistic = 2 muscles opposite e/o

concentric

shortening of the muscle

eccentric

lengthening of the muscle

example: elbow joint

flexes as biceps contract/triceps extends the elbow (antagonists)

sarcolema

muscle membrane

sarcoplasm

muscle cytoplasm

sarcomere

muscle segment

striations

stripes formed from repeating series of dark and light bands along length of each myofibril

muscle organ

bundle of fascicles

fascicle

bundle of muscle fibers

myofibril

individual muscle fiber, thick/thin filaments

epimysium

surrounds entire muscle, outer-most

perimysium

surrounds fascicles, middle

endomysium

surrounds individual muscle fibers, inner-most

titin

a protein that positions the myosin filament to maintain equal spacing between actin filaments

thin filaments

I bands (light)

thick filaments

A bands (dark)

Z-disc

edge of a sarcomere, center of an I-band

M-lines

center of A band to hold down thick filaments

duchenne muscular dystrophy (DMD)

most common form of muscular dystrophy; affects primarily men because it is X-chromosome linked (mother to son)

- dystrophin mutation: dystrophin is just under sarcolemma, causes weakness and deformity

sliding filament theory

theory that actin filaments slide toward each other during muscle contraction, while the myosin filaments are still

- length-tension relationship: optimal overlap of thick/thin filaments

cross bridge cycle

1) ADP bonds to myosin head in a cocked position, ready to bind to actin and is covered in tropomyosin

2) Ca2+ binds to troponin which moves tropomyosin off of actin bind site

3) bound myosin forms cross-bridge to rotate head toward center of sarcomere, produces "power stroke"

4) ADP is released, ATP binds to myosin head and cross-bridge detaches

**Need ATP. If no ATP, then myosin stays bound and causes rigor mortis or body stiffness.

sarcoplasmic reticulum

modified smooth ER, stored Ca2+ internal to muscle until it's needed

transverse tubules

system of tubules that provides channels for ion flow (Ca2+) throughout the muscle fibers to facilitate the propagation of an action potential.