metabolic and nutritional mechanisms Flashcards
protein energy metabolism (PEM)
- lead to malnutrition
- increase susceptibility to infectious diseases
- determined by body mass index - malnutrition below 16
marasmus
PEM syndrome
- somatic protein –> proteins in skeletal muscle
- prevent loss of visceral protein, but depleted carbs
- growth retardation, emaciation, large head, immune deficiency, anemia
kwashiorkor
PEM syndrome
- visceral protein –> proteins in visceral organs (ex. liver)
- loss of visceral protein, but have plenty of carbs
- edema, swollen abdomen due to hypoalbuminemia and fatty liver, hypovolemic shock, heart failure
cachexia
occur with tumors and chronic inflammatory rxns
-proteolysis inducing factor (PIF) and pro inflammatory cytokines (TNF, IL-6) –> skeletal muscle breakdown via NFkB activation of proteasome
anorexia nervosa
self induced starvation
- severe PEM with effects on endocrine system
- amenorrhea from low GnRH, LH, FSH
- decreased thyroid hormone and bond density
- cardiac arrhythmia and sudden death
bulimia
binging on food and induced vomiting
-menstrual irregularities, electrolyte imbalances, pulmonary aspiration, esophageal and gastric rupture
fat soluble vitamins
- stored in adipose and liver
- not excreted –> vit. A, D can build up and become toxic
folic acid (vitamin B9)
- needed for maturation of hematopoietic cells
- deficiency common in alcoholics and pregnancy
- can make RNA, but not DNA –> megaloblastic anemia
- can become deficient quickly
vit. B12 (cobalamin)
- associated with folate
- convert homocysteine to methionine
- degrades FAs –> accumulation of FAs (neurologic conditions) if deficient
- important for neurological function
- long stores in body - not deficient quickly
- pernicious anemia w/ no parietal cells or IF
microcytic vs. macrocytic anemia
microcytic –> vit. B6 deficiency
macrocytic –> vit. B9 deficiency
pyridoxine deficiency (vit. B6)
- coenzyme for amino acid metabolism
- deficiency –> microcytic anemia
- toxicity –> sensory neuropathy
thiamine (vit. B1)
- decarboxylation rxns and energy metabolism in nervous system
- wernicke Korsakoff –> memory loss, loss of balance
- beriberi (sever) –> wet (cardiovascular) or dry (nervous system); tachycardia, convulsions, confusion, paralysis
niacin (vit. B3)
- coenzymes in oxidation/reduction rxns (OXPHOS, ETC)
- deficiency –> pellagra
- supplementation lowers VLDL, LDL and increase HDL
riboflavin (B2)
- active forms of FMN and FAD
- coenzymes for oxidation/reduction rxns
biotin (B7)
- coenzyme for carboxylation rxns (carry CO2)
- supplied by intestinal bacteria
pantothenic acid (B5)
-CoA –> transfer acyl groups
vitamin A (retinol)
vision, reproduction, growth, epithelial tissues
- stored in liver, bound to retinol binding protein
- absorbed by bile and pancreatic enzymes –> chylomicrons and apolipoprotein E
major functions of Vitamin A
- maintain normal vision
- rhodopsin for night vision
- photopsins for color vision - cell growth and differentiation
- epithelial growth and differentiation
- retinoids used for acne, psoriasis, and acute promyelocytic leukemia
deficiency and toxicity of vitamin A
- deficiency
- night blindness, epith. metaplasia and keratinization, xerophthalmia, bitot spots, keratomalacia, respiratory and urinary tract infections - overdose
- liver cirrhosis, teratogen
vitamin D
- 1,25 dihydroxycholecalciferol (active)
- ergocalciferol in plants, D2
- cholecalciferol in animals, D3
- most formed from UV exposure
- PTH dependent to convert to final active form in kidney
metabolism of vit. D
- can get D3 from diet or UV light
- bind to vit. D binding protein to transport to liver
- increase Ca++ and phosphate absorption in small intestine
- increase RANKL in osteoblasts –> activate osteoclasts and produce osteocalcin
- regulate in kidney by 1alpha-hydroxylase
- maintain plasma Ca++
- prevent hypocalcemia tetany etc.
deficiency and toxicity of vit. D
- deficiency - osteomalacia and rickets
2. toxicity - renal stones
vitamin C (ascorbic acid)
antioxidant and hydroxylation of collagen
- need collagen for stable helical configuration
- deficiency –> scurvy and hemorrhage
- toxicities –> Fe overload, hemolytic anemia, kidney stones
vitamin K
blood clotting factors
-antibiotics can inhibit gut bacteria production of vit. K leading to malnourishment and bleeding
vitamin E
tocopherols
- antioxidants
- deficiency –> susceptible to oxidative stress
- does not help with CV disease
3 hormones for regulating satiety and appetite
- ghrerlin - secreted by stomach, stimulates appetite
- leptin - secreted by adipocytes, decrease appetite
- insulin, CCK, peptide YY - produce satiety
leptin
- increase sensitivity to brain for satiety signals
- deficiency –> overeat
- stimulated when fat stores are abundant
adiponectin
fat burning molecule
-injections can stimulate fatty acid oxidation causing a decrease in muscle mass
ghrelin
- produced in stomach and hypothalamus
- only one that increases food intake
- suppression of ghrelin in obese –> overeating
- PYY and amylin inhibit neurons decreasing food consumption
adipocytes
produce cytokines that produce pro-inflammatory states leading to atherosclerosis
consequences of obesity
- metabolic syndrome - increase risk for cardiovascular disease and diabetes
- high risk for gallstones, hypoventilation, osteoarthritis
- increased IGF-1 leading to proliferation and inhibit apoptosis leading to tumor
- hypercholesterolemia –> atherosclerosis
