Chapter 21: Obesity, Starvation, and Anorexia of Aging
white adipose beige adipose brown adipose
adipose tissue (3)
anorexia of aging
adverse outcomes: malnutrition frailty mitochondrial dysfunction reduced regenerative capacity increased oxidative stress imbalanced hormones
visceral obesity
around abdomen distribution of body fat is localized around the abdomen and upper body "apple shape" associated with more obesity complications than peripheral
hypothalamus
balances opposing effects of neurons
long-term starvation
begins after several days of dietary abstinence (therapeutic & pathologic) causes death from proteolysis marasmus kwashiorkor cachexia refeeding syndrome
refeeding syndrome
body adapts to starvation (homeostasis) << nutrition after starving << too much nutrients too fast << electrolyte imbalance
excess WAT
causes dysregulation of secretion and function of adipokines
adipokines
cell signaling proteins function like hormones
food intake and energy balance
controlled by central and peripheral physiological signals
anorexia of aging
decrease in appetite or food intake in older adults aging associated with decreased orexigenic signals and increased anorexigenic signals
starvation
decreased energy intake leading to weight loss
White Adipose Tissue (WAT)
derived from CT single lipid droplet located in visceral (central) and subcutaneous (peripheral) stores, muscles, and bone marrow
brown adipose tissue (BAT)
derived from muscle tissue multiple lipid droplets, rich in mitochondria generate heat through oxidation of fatty acids and glucose (neonatal heat generation/protects against obesity)
peripheral obesity
distribution of body fat is extraperitoneal and distributed around the thighs and buttocks "pear shape"
malnutrition
doesn't have to be starving lack of nourishment from inadequate amounts of calories, protein, vitamins/minerals caused by diet, alterations in digestion/disease
short-term starvation
extended fasting, several days of dietary abstinence/deprivation---- therapeutic: initial rapid weight loss body responds to protect protein mass (glycogenolysis & gluconeogenesis)
adipocytes
fat storing cells secrete proteins acts like endocrine (secretes hormones)
beige adipose tissue
found in WAT but multiple mitochondria like BAT emerge with chronic exposure to cold/exercise diminished in obesity
bone marrow adipose tissue (MAT)
found in all bones increases with obesity and age
metabolic syndrome
hyperglycemia << access fat around waist << abnormal cholesterol << high blood pressure << higher risk for heart attack /stroke
obesity
increase in body adipose tissue body mass index greater than 30 kg/m2 for adults; caloric intake exceed caloric expenditure in genetically susceptible people
adipose
insulation mechanical support secretes adipokines immune cell function immune cell function energy reserve
obesity patho
interaction of peripheral and central pathways and numerous adipokines, hormones and neurotransmitters signaling medication acts on hypothalamus and brainstem to regulate hunger and satiety
adipokines
leptin adiponectin retinol-binding protein 4 endocannabinoids angiotensinogen ghrelin glucagon-like peptide 1 peptide YY cholecytokinin
increase hunger, increase insulin resistance, increase inflammation
leptin adiponectin retinol-binding protein endocannabinoids angiotensinogen (increase vasoconstriction)
obesity
major cause of death: cardiovascular disease type 2 diabetes mellitus cancer
cachexia
muscle atrophy and weight loss from loss
normal weight obesity
normal body weight and BMI with percent of body fat greater than 30%
metabolically healthy obesity
obese but have no metabolic-obesity associated complications and decreased risk for morbidity and mortality look obese but do not have symptoms of metabolic syndrome
obesity
produces state of chronic; low-grade inflammation in WAT (insulin resistance, metabolic syndrome, other comps) alterations in intestinal microbiome weight loss (bariatric) surgery is the most effective treatment for decreasing obesity-related morbidity
orexigenic neurons
promote appetite, stimulate eating, decrease metabolism
kwashiorkor
protein deprivation with carbohydrate intake; water bloating
marasmus
protein energy malnutrition
white adipose tissue
release free fatty acids and glycerol for energy metabolism = diabetes mellitus type 1 = has body in glucose but doesn't have insulin to use energy = breaks down fats = release acids and ketones = diabetic ketoacidosis
anorexia of aging
risk factors: functional impairments medical and psychiatric conditions loneliness and grief; social isolation abuse/neglect treatment: support
obesity
risk factors: polygenic defects metabolic abnormalities environmental factors depression and mood disorders
adipocytes
secretes adipokines
GI tract
secretes hormones that control hunger and satiety
anorexigenic neurons
suppress appetite, inhibit eating, increase metabolism
