TEST 4: Obesity Flashcards

1
Q

Obesity overview
(Lecture, p. 723)

A

-A metabolic disorder that develops when calorie intake exceeds caloric expenditure in genetically susceptible individuals

-In adults, obesity= BMI > 30
-Class 1: BMI 30 to < 35
-Class 2: BMI 45 to < 40
-Class 3: BMI > 40 “severe”

-In kids:
-BMI > 95th percentile for age and gender
—120% of 95% peregrine or greater OR 35 kg/m2 or greater

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2
Q

Obesity overview
(Lecture, p. 723)

A

-A metabolic disorder that develops when calorie intake exceeds caloric expenditure in genetically susceptible individuals

-In adults, obesity= BMI > 30
-Class 1: BMI 30 to < 35
-Class 2: BMI 45 to < 40
-Class 3: BMI > 40 “severe”

-In kids:
-BMI > 95th percentile for age and gender
—120% of 95% peregrine or greater OR 35 kg/m2 or greater

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3
Q

Adipose tissue
(P. 723)

A

-Provides insulation and mechanical support
-Body’s major energy reserve to fuel other tiessuss

4 types:
-White
-Brown
-Beige
-Bone marrow

GEM- MOST fat in the body is white

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4
Q

White adipose tissue
(P. 723)

A

-Comprises the majority of adipose tissue

-Located in visceral (central) and subcutaneous (peripheral) stores

-Contributes to the regulation of energy homeostasis:
-Adipocytes are fat storing cells that store energy as triglycerides, synthesize it from glucose, and mobilize energy from free fatty acids and glycerol
-Secrete adipokines (hormone like cytokines) that are secreted to regulate metabolic function and immune response

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5
Q

Adipokines deregulated vs.
Adipocytes regulated

A

Adipokines:
Leptin, adiponectin, resistin, RBP-4 when deregulated:
-HTN, CVA. Obesity, arthritis, DM, Arthritis, metabolic syndrome, NASH

Adipocytes when regulated (a million types listed):
-Appetite, satiety, insulin sensitivity, fat distribution, energy, blood pressure, metabolic health

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6
Q

White adipose tissue
(P.723)

A

When the energy balance is positive, excess fat is stored in white Adipocytes:

-Cells hyper trophy and become hyper plastic
-Causes dysregulation of adipokines—> pro inflammatory state and altered lipid metabolism—> contributes to obesity comorbidities

Altered Adipocytes—> insulin resistance (lipolysis and release Of FFA)—> macrophage infiltration (TNF-alpha and IL-6)

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7
Q

Other adipose tissues
(P.723)

A

Brown:
-Composed of mitochondria and iron (brown color)
-Generates heat (higher in neonates than adults)
-Does not play a role in appetite or satiety (no negative metabolic effects)
-No shivering thermogenesis

Beige:
-Appears in extreme cold or with exercise
-Protective against obesity, increases energy expenditure and weight loss

Bone marrow adipose tissue:
-In all bones (particularly long bones)
-Releases adipokines with osteoblast activity (excess osteoporosis and inflammation associated with RA)

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8
Q

Appetite and satiety

A

-Controlled by arcuate nucleus in the hypothalamus (responsibly for balancing metabolism)

Orexins= appetite stimulation

Anorexins = appetite inhibitor

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9
Q

Orexins
(P. 727)

A

Ghrelin:
-Produced in the stomach in response to hunger
-Ghrelin receptors in hypothalamus—> growth hormone that—> release gastric acid, increases GI motility, pancreatic secretion of insulin
-Lean people: elevate with hunger and fall after eating
-In obesity: levels remain elevated after eating (increased body weight and fat mass)

Endocannabinoids:
-Produced in the brain and peripheral nerves
-Increases appetite, nutrient absorption and lipogenesis
-Increases peripheral and central adipose tissue accumulation

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10
Q

Anorexins
(P.726)

A

Leptin:
-Produced by Adipocytes, acts on hypothalamus
-Decreases appetite and energy expenditure
-As Adipocytes increase, Leptin secretion increases
High levels of Leptin lose effectiveness (Leptin resistance) —> disrupts hypothalamus signals of satiety—> overeat—> increased weight

Glucagon-like Peptide-I :
-Stimulates pancreatic glucose dependent insulin secretion
-Decreases gastric emptying—> decreased appetite and increased satiety

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11
Q

Adiponectin
(P. 726)

A

-An Anorexin, increases energy expenditure
-Has insulin sensitizing and anti inflammatory properties
-Levels will decrease in obesity—> increased insulin resistance, increased CAD risk, and increased inflammatory markers.

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12
Q

Shifts in obesity from normal
Hunger

A

Ghrelin and endocannabinoid—> does NOT decrease after eating, so you lose the feedback loop to trigger hunger (increases appetite)

Leptin, GLP-I, adiponectin—> levels are high but three lower is resistance, so you lose the signal to stop eating, lose the satiety sensor, and lose protective properties

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13
Q

Apple V pear shape obesity

A

Apple:
-VISCERAL obesity: accelerated lipolysis, increased inflammation and metabolic syndromes

Pear:
-PERIPHERAL obesity: fat is less metabolically active, releases fewer adipocytokines—> risk of obesity is less severe

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14
Q

Obesity as multi-system syndrome

A

-Chronic complications are associated with > 200 health conditions
-Underlying etiologies: chronic inflammation, metabolic disorders, increased free fatty acids

Cardiovascular: Atherosclerosis, HTN, CAD, HF, renal disease, CVA

Cancer: Breast, colon, renal, stomach, pancreatic, liver, ovarian/ endometrial

GI: GERD, gallstones, fatty liver

Pulmonary: Sleep apnea, asthma exercise intolerance

Musculoskeletal: osteoarthritis, back pain, plantar fasciitis

Endocrine: insulin resistance, type 2 DN,
Infertility

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15
Q

Obesity treatment

A

-Is a chronic, relapsing disease

Treatment focus areas:
-Address metabolic abnormalities
-Lifestyle change
-CBT/ support groups
-GLP-I and GIP receptors agonists
-Bariatric surgery (Gastric bypass, roux-en-Y, gastric banding, gastric sleeve)

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