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KIN 404 Test 1 ARTICLE NOTES.docx

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Department
Kinesiology
Course Code
KIN 404
Professor
Russ Tupling

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Cellular bioenergetics as a target for obesity therapy  Obesity = EI > EE  Standard metabolic rate/BMR - rate of energy utilized by an organism in the awake resting state but not actively digesting food and at thermoneutrality.  Adaptive thermogenesis – heat caused by responses by body to cold temperature and diet. o Primary sites of action = mitochondria of skeletal muscle and BAT  Losing weight only by calorie restriction: o Mammals designed to guard against starvation = redundant systems in place to overcome suppression of one pathway, therefore drug won’t have long term effect. o Central satiety centers often interconnect with other core regulations in the brain causing phsycotropic side effects. o Body has homeostatic mechanism such that weight loss produces an increase in calorific efficiency = decreases BMR making further weight loss more difficult.  Bioenergetics – studies the flow of chemical bond energy within organisms. o Takes place in mitochondria where energy from nutrients is released through the tricarboxylic acid cycle and ETC. Oxygen is consumed, water + CO2 + ATP produced.  ATP distribution throughout the cell: o Maintenance of Na/K and Ca pumps (30%) o Protein synthesis (30%) o Gluconeogenesis, ureagenesis, turnover of CHO and lipid stores (20%)  Interconversion process = inefficient o Heat lost even in tightly coupled reactions  Entirely uncoupled reactions in humans (thermogenic/energy consuming): o In all cells, H, Na, K and Ca leak back across membrane channels down electrochemical gradients. o In mitochondria, proton leak ~ 20% o Muscle tissue:  Inwardly rectifying Ca and Na channels  Cycling of actin-myosin during contraction and relaxation  Physical work  Triglyceride/fatty-acid cycling (esterification of TG is followed by hydrolysis) o Regulated proton leak in BAT by UCP1  UCP1 – inner mitochondrial trans membrane protein expressed only in brown adipocytes  UCP1 deficient mice = sensitive to cold temperatures, increased risk to diet induced obesity  Transgenic mice with UCP1 expression in white fat = lean phenotype  UCP2 – expressed at low levels, UCP3 – expressed preferentially in skeletal muscle. Adaptive thermogenesis  Genetic factors account for 50-90% of variance in weight gain (diff in EE and adaptive thermogenesis)  In mammals, occurs in BAT and skeletal muscle.  3 subtypes: o Shivering thermogenesis – caused by cold exposure, function of skeletal muscle o Non-shivering thermogenesis – function of brown fat  Prolonged cold – even as shivering stops, EE remains elevated.  Newborns do not shiver and maintain body temp by non-shivering brown fat  Heat produced used to maintain body temp o Diet-induced thermogenesis – triggered by overfeeding, function of brown fat  Luxuskonsumption = a physiological mechanism exists that permits excessive calorific intake to be dissipated as heat, allowing individuals to eat without gaining weight.  Closely associated with recruitment of BAT by enhanced adregenic activity  Heat produced quickly dissipated to environment to prevent rise in body temp  Pair-fed genetically obese mice – defect in BAT mediated thermogenesis  UCP1 ablated mice = more susceptible to cold temp and have to rely on shivering  UCP1 KO mice at thermoneutrality = lack diet induced thermogenesis and develop obesity o Diet induced thermogenesis is fully independent on UCP1 Neuronal and hormonal regulation of adaptive thermogenesis  Hypothalamic nuclei in CNS integrate stimuli from 2 separate pathways to reg thermogenesis o Feed-forward pathway involving cutaneous thermal receptors acting via thermosensory neurons  Cause GABA-ergic interneurons in dorsomedial hypothalamus to disinhibit thermogenesis-promoting neurons in DMH and driving non-shivering in BAT o Negative FB pathway involving temp-sensitive neurons in brain  Inhibit SNS outflow to BAT  Adaptive thermogenesis is regulated primarily by SNS. o Noradrenaline released from SNS regulates brown adipocytes o Promotes proliferation and differentiation of brown adipocytes o Directly regulates the thermogenic program of BAT by activating UCP1 o Protects brown adipocytes from TNF-alpha induced apoptosis  Adaptive thermogenesis is also modulated by hormones o Type 2 iodothyronine deiodinase – regulates amount of active T3 in brown fat o Leptin, released by white adipocytes – regulates energy balance by effects on hypothalamus
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