Week 1: Energy and Organic Matter Balance-Obesity Flashcards
1
Q
Obesity and fuel composition
A
- obesity arises if body fails to properly adjust the composition of fuel the body burns in response to the composition of fuel ingested from food
- If relative amount of fat the body burns is less than relative amount in the food, then an increase in relative body fat content may result
2
Q
RQ and FQ and obesity
A
- RQ: amount of CO2 produced divided by amount of O2 consumed for living organisms
- FQ: for organic matter absorbed from food
- for fat RQ=0.7, for carbs RQ=1.0
- when RQ>FQ can lead to obesity. Indicates fat content of ingested food exceeded fat content of metabolized food
3
Q
Absorptive state characteristics
A
- Carb, mainly glucose and fructose, as major source of energy for all cells. RQ approaches 1
- Net synthesis of protein from amino acids
- Net storage of glycogen in liver and muscle
- Net storage of TG, particular in adipose tissue
- glycerol-3-P not glycerol is source of glycerol in TG. Carbs that undergo kerb cycle is source of glycerol-3-P
- adipocytes lack glycerol kinase - Conversion of amino acids and carb into FAs
- anaerobic glycolysis of carbs can increase relative fat content of organism
4
Q
Characteristics of post absorptive state
A
- utilization of FAs as major energy source; spared combustion of glucose. Except in nervous tissue and RBCs which still use glucose.
- Increased circulating levels of FA acts on muscle to decrease glucose utilization. RQ approaches 0.8 - Net release of FAs from adipose tissue
- Maintenance of blood glucose levels via hepatic glucose production
- gluconeogenesis and glycogenolysis - Net protein degradation with hepatic conversion of amino acids to glucose
5
Q
Starvation state
A
-after utilizing glycogen stores in liver and gluconeogenesis from lactate or amino acids from muscle, nervous tissue starts using ketoacids from fat
6
Q
Insulin and absorptive state
A
- promotes glucose uptake into muscle. Glucose is phosphorylated once it enters muscle, and can’t leave b/c muscle lacks Glucose-6-phosphatase
- promotes muscle combustion of CHO and reduces utilization of fat - Promotes glycogen accumulation, mainly in muscle and fat, but also liver
- Promotes amino acid uptake and protein accumulation, particularly in muscle. Reservoir of AAs for later conversion to glucose by liver
- promotes TG storage in adipose tissue
- glucose into adipocytes, supplies glycerol-3-P
- insulin promotes dephophorylation and deactivation of HSL (hormone sensitive lipase)
- promotes fat accumulation - decreases glucagon release
7
Q
Insulin regulation: promoters
A
STIMULATES INSULIN RELEASE
- food ingestion, vagal neurons promote insulin release
- incretins released from gut (distinguishes rise of glucose from hepatic glucose output in fight or flight response)
- GLP1: lowers blood glucose by increase insulin release, suppresses glucagon
- DPP-4 inhibitors inhibit degradation of GLP-1
8
Q
Insulin regulation: Inhibition of secretion
A
- somatostatin produced by pancreas
- sympathetic control: Norepinephrine and epinephrine act via a-adrenergic receptors, inhibit insulin release
9
Q
hyperinsulinemia and obesity
A
- hypothesis: hyperinsulinemia is a cause of obesity
- insulin secretion is pulsatile, pulses are greater in the obese
- insulin resistance: obese persons need greater amounts of insulin for effects
10
Q
Tissue selective regulation of insulin effectiveness
A
- amylin (found in amyloid deposits in pancrease of type 2 DM): inhibited insulin stimulated glucose uptake and glycogen deposition in muscle
- idea: an amylin inhibitor might potentiate insulin action on muscle but not fat, could decrease insulin levels and decrease adipose mass
- exercise actually does that: makes muscle uptake of glucose more insulin sensitive, possibly due depletion of muscle glycogen stores. Exercise shifts fuel utilization at a rest toward fat oxidation
11
Q
Glucagon and post-absorptive state
A
- fall in glucose is main stimulus of release of glucagon. Opposes action of insulin on liver and fat
1. promotes release of fatty acids from adipose tissue - increase cAMP and promotes phosphorylation of HSL. TGs broken down to FAs
- flow of FAs to muscle decreases combustion of glucose
2. promotes release of glucose from liver - glucagon increases phosphorylation of glycogen synthase and phosphorylase
- glycogenolysis and glucose release
12
Q
Epinephrine and post absorptive state
A
- promotes release of FA from adipose tissue
- Promotes release of glucose from liver
- acts on muscle to decrease insulin action, promotes glycogenolysis and lactate efflux
- promotes glycogen and inhibits insulin release
- promotes blood flow through adipose tissue, lipolysis, and FA efflux
13
Q
CNS and regulation of energy and organic matter balance
A
- lesions to lateral hypothalamus: cause anorexia and adipose wasting
- lesions to VMH: cause overeating and obesity
- ob/ob mice: leptin deficient. Obese
- db/db and Zucker rat: obese, high leptin, dysfunctional leptin receptor
- leptin: inhibits glucagon release
14
Q
Gut as neuroendocrine organ
A
- distension and composition of food cause signals to brain and other organs to regulate eating behavior
- GPCRs in mouth coupled to G protein to provide taste. Also found in gut, regulate release of GLP-1 from gut.
- ghrelin: hormone from gut, “hunger hormone”
15
Q
Thermogenesis form oxidation uncoupled from activity
A
- in brown adipose tissue (BAT), found uncoupling protein (UCP) that uncouples oxidation from generation of ATP. Oxidation produces heat.
- mild cold exposure increases human BAT glucose consumption. Agents that mimic cold activation BAT thermogenesis my be Rx for obesity
- hypothesis: tissues other than white adipose tissue, such as muscle and BAT, may produce endocrine signals indicating status of their energy reservoir and that aberrations involving them may contribute to obesity
