Chapter 24: Metabolism and Nutrition Flashcards

1
Q

Metabolism:

A

All the chemical reactions that take place in the body.

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2
Q

Catabolism:

A

Breaking down complex molecules. Release energy (providing ATP).

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3
Q

Anabolism:

A

Making complex molecules. Requires energy (uses ATP).

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4
Q

ATP:

A

Adenosine triphosphate= energy currency of the cell.

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5
Q

Nutrients:

A

o Substances in food used by the body to promote growth, maintenance, or repair of body tissues.
o 6 Classes: Carbs, proteins, lipids, vitamins, minerals, and water.

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6
Q

Essential Nutrients:

A

o Specific nutrients that our body either can’t make or can’t make in sufficient amounts to meet the body’s needs.
o Essential amino acids:
o 8 a.a. that adults cannot make (10 in infants)
o Found in “complete” = “high quality” proteins = proteins that contain the optimal ratio of these essential a.a.
o Essential fatty acids:
o Linoleic and possibly linolenic fatty acids.
o Most vitamins, some minerals, of course water, and enough calories to sustain life (from carbs, pro, fats).

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7
Q

Essential Amino Acids:

A

o Essential a.a. are not stored in body.
o Body proteins are made in cells with an “all or nothing” system. If even one a.a. is not available, the protein cannot be made at that point in time, e.g., translation comes to a halt!
o Examples of high quality (complete) proteins = eggs, meats (all types), dairy products.
o Vegetables supply incomplete proteins!!!

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8
Q

General Functions of Macromolecules:

A
o	Supply energy via oxidation:
o	Carbs:  4 kcals/gram.
o	Proteins:  4 kcals/gram.
o	Fats:  9 kcals/gram.
o	ETOH:  7 kcals/gram.
o	Serve as building blocks for synthesis:
o	Tissue repair and wound healing.
o	Growth, pregnancy, lactation.
o	Stored for future use: Carbs as glycogen; fats as TG.
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9
Q

Metabolic Pathways:

A

About 40 percent of energy in original bonds captured as ATP, the rest is dissipated as heat.

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10
Q

Storage of Macromolecules:

A

o Carbs are stored as glycogen primarily in liver and muscle cells (all cells can store a limited amount of glycogen).
o Glycogen can NOT be transported in the blood!!!!!
o Fats are stored as triglycerides (TG):
o Excess carbs can be converted to TG.
o Excess proteins can be converted to TG.
o Excess fats can be converted to TG.
o However, fatty acids can NOT be converted to glucose (glycerol can be).

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11
Q

Carbohydrates:

A

o General Functions:
o Glucose is major body fuel in the FED state.
o Glucose can be used by all body cells.
o Glucose is only energy source for neurons and RBCs (in normal metabolic states).
o Pentose sugars are used to make nucleic acids.
o Glycoproteins and glycolipids are part of cell membranes.
o Source of dietary fiber and nutrients.
o 440 grams of carb stored in body.
o Requirements:
o Minimal requirements are not known.
o Dietary Reference Intake for adults is 130 grams of carbs/day.
o 75 to 100 grams of carb/day thought to be needed by most humans to maintain adequate blood glucose levels and to avoid ketosis.
o Typical American diet = 200 to 400 grams of carb/day (about 46 percent of kcals).
o We consume 60 lb. of table sugar and 46 lb. of corn syrup/year (100 years ago, only 4 lb. of sugar/year!!!).
o Highly active people need more carbs!

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12
Q

Glycolysis:

A

Converts glucose to pyruvic acid.

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13
Q

Glycogenesis:

A

Polymerizes glucose to form glycogen (simply put: making of glycogen).

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14
Q

Glycogenolysis:

A

Breaking glycogen down to glucose.

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15
Q

Glucogenolysis:

A

Forms glucose from noncarbohydrate precursors.

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16
Q

Lipolysis:

A

Breaks down lipids to fatty acids and glycerol.

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17
Q

Lipogenesis:

A

Forms lipids from acetyl CoA and glyceraldehyde phosphate.

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18
Q

Lipids:

A

o Dietary Sources:
o Fatty acids that make up the TG in our food can be saturated, monounsaturated, or polyunsaturated.
o Cholesterol comes primarily from animal foods.
o General Function
o Oxidized (catabolized) to make ATP.
o Helps body absorb fat-soluble vitamins.
o Slows gastric emptying—satiety!
o Phospholipids/cholesterol important structural component of cell membranes.
o Adipose tissue cushions body organs.
o Temperature regulation.
o Cholesterol used to make bile, steroid hormones and precursor to Vitamin D.
o Requirements:
o No minimum except for essential fatty acids.
o Body makes cholesterol!
o There are suggested LIMITS to fat intake.

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19
Q

Cholesterol:

A

o Sources of cholesterol in the body
o Food (eggs, dairy, organ meats, meat).
o Synthesized by the liver and intestinal cells.
o Saturated fat = F.A. with no double bonds (carbons completely “saturated” with hydrogen atoms).
o Hydrogenation.
o Trans-fatty acids.

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20
Q

Important Terms in Lipid Metabolism:

A
o	Oxidation of Fat (breakdown of fat to make ATP).
o	Lipolysis:  TG turns into  F.A.+ glycerol.
o	Beta oxidation:  breaking F.A. down into 2-carbon fragments that can enter the Kreb’s cycle.
o	Lipogenesis (making fat/TG).
o	Ketogenesis (production of ketones).
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21
Q

Oxidation of Fat:

A

o LIPOLYSIS = breaking a TG down into glycerol + fatty acids (F.A.).
o F.A. are then broken down into 2-carbon fragments (acetyl CoA) to enter Kreb’s cycle=BETA OXIDATION.
o F.A. are the preferred energy fuel for:
o Liver, Heart muscle, Skeletal muscle.

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22
Q

Proteins:

A

o Dietary sources
o Complete: contains all 8 essential a.a. in optimal ratio.
o Incomplete: missing at least one essential a.a.
o General functions of proteins:
o Amino acids are the building blocks for all our important body proteins:
o Structural proteins (keratin, collagen)
o Hormonal proteins (insulin, glucagon, etc.)
o Enzymes
o Transport/carrier proteins
o Contractile proteins
o Defensive proteins (Ab, complement, interferons, etc.)
o Histone proteins wrapped around DNA
o Need the NITROGEN of amino acids to make: Purines and pyrimidines, Creatine, Porphyrins (Hb, myoglobin, cytochromes).
o Requirements:
o Need to eat enough protein to stay in nitrogen balance.
o Adults need 0.8 grams of protein per kg of ideal body weight.

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23
Q

Nitrogen Balance:

A

o Our bodies do NOT store nitrogen, must be obtained from dietary protein or from recycling N-containing compounds already in the body.
o Nitrogen balance:
o Amount of nitrogen ingested in proteins =Amount of nitrogen excreted in feces/urine.
o Positive Nitrogen Balance (more protein synthesis than protein breakdown):
o Growth in childhood.
o Pregnancy and lactation.
o Repair of tissues after illness or trauma.
o Skeletal muscle hypertrophy.
o Negative Nitrogen Balance (protein breakdown exceeds protein synthesis):
o Starvation.
o Physical stress (trauma, surgery, burns, infections).
o Emotional stress (severe depression/anxiety).

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24
Q

Skeletal Muscle Hypertrophy:

A

o Must stress the muscles (eccentric contractions that tear myofibrils).
o Must eat adequate amounts of protein.
o Must eat adequate kcals (so protein can be used to BUILD rather than being burned/oxidized to make ATP).
o Must eat adequate carbs so insulin can drive a.a. into the skeletal muscle cells.
o Must have adequate REST.

25
Q

Tissue Repair/Wound Healing:

A

o Scar tissue contains a lot of collagen.
o Must eat adequate amounts of protein.
o Must eat adequate kcals (so protein can be used to BUILD rather than being burned/oxidized to make ATP).
o Must eat adequate carbs so insulin can drive a.a. into cells needing repair.
o Must have adequate REST.
o Need extra amount of Vit. A and C, zinc.

26
Q

Vitamins:

A

o Dietary sources: varies/each vitamin.
o Fat-soluble vitamins (A, D, E, K).
o Water-soluble vitamins (C and B vitamins).
o General functions of vitamins:
o NOT used as fuel to make ATP.
o Most fxn as COENZYMES that help an enzyme catalyze a specific chem. Reaction.
o Vit D probably important for immune fxn.
o Antioxidant vitamins probably play a role in preventing cancer and CVD.
o Requirements: varies/each vitamin.

27
Q

Hyper vs. Hypovitaminosis:

A

o Concept: 5X the Recommended Dietary Allowance is probably better considered a DRUG dose rather than a nutrient intake.
o Hypervitaminosis A (usu. More than 20,000 IU/day)
o N and V, fatigue, H/A, blurred vision, anorexia, reddening and exfoliation of skin, bone and jt. pain, enlargement of liver/spleen, birth defects
o Hypervitaminosis D (usu. More than 10,000 IU/day)
o Fatigue, weight loss, hypercalcemia, calcification of soft tissues, heart and kidney damage.
o Hypervitaminosis B-6 (usu. More than 200 mg/day).
o Ataxia, severe sensory neuropathy, nerve damage.

28
Q

Minerals:

A
o	Dietary Sources:  varies/each mineral.
o	NOT found in most fats, sugars, refined carbohydrates.
o	General functions of minerals:
o	NOT used as fuel to make ATP.
o	Electrolytes.
o	Provide strength to some tissues (bone).
o	Cofactors for enzymes.
o	Requirements:  varies/each mineral.
29
Q

Metabolism Pathways:

A

o Metabolism in FED (“absorptive”) state:
o Period in the first few hours after eating where energy sources are supplied by the breakdown of food you just ate.
o Metabolism in UNFED (“post-absorptive”) state:
o Period when digestive tract is empty and energy sources are supplied by the breakdown of body stores and reserves.

30
Q

Metabolism in Absorptive (Fed) State:

A

o Absorptive state = “fed”state = first few hours after eating.
o General facts:
o Building processes (anabolism) exceeds breaking down processes (catabolism).
o STORAGE of fuel is emphasized.
o SYNTHESIS of important body compounds (making glycogen, TG, important proteins).
o Anabolic processes require ATP.
o Glucose is the major energy fuel to make ATP in the fed state (glycolysis/Kreb’s).

31
Q

Carb Metabolism in Fed State:

A

o Carbs absorbed and delivered to liver as monosaccharides (mostly glucose).
o Liver has choices about what to do with that glucose:
o Hepatocytes oxidize glucose to make ATP.
o Store glucose as glycogen (glycogenesis).
o Convert excess carbs to TG released into blood as VLDL’s.
o Send glucose on to other body cells.
o 50 percent is oxidized by your body cells to make ATP via glycolysis/Kreb’s cycle/ETS.
o 40 percent is converted to TG and stored either inside body cells or in the TG of adipose cells.
o 10 percent is stored as glycogen in liver and in muscle tissues.
o 100 grams stored in liver.
o 325 grams stored in muscle.

32
Q

Lipid Metabolism in Fed State:

A

o Lipids are sent to liver as free F.A. in blood (short-chain F.A.) or as chylomicrons made by intestinal cells.
o As chylomicrons travel in the blood, they are broken down by an enzyme called LIPOPROTEIN LIPASE, very active in the capillaries serving adipose tissue and muscle cells.
o The liver easily makes TG and transports it to other body cells via VLDLs (very low density lipoproteins).

33
Q

Lipoproteins:

A

o Lipoproteins are transport vehicles for fatty substances that otherwise are not soluble in the blood.
o Lipoproteins carry TG, cholesterol, phospholipids, and some protein.
o Each type of lipoprotein has a different structure and a very specific function!
o Chylomicrons, VLDL, LDL, HDL.
o Structures:
o Chylomicrons—mostly TG.
o VLDL—mostly TG and cholesterol.
o LDL—mostly cholesterol.
o HDL—mostly protein.
o Functions:
o Chylomicrons deliver dietary fat to body cells after absorption in the gut.
o VLDL’s deliver fat the liver has made to other body cells (as it lets go of the TG, it morphs into an LDL with mostly cholesterol).
o LDL’s deliver cholesterol to body cells (receptor-mediated endocytosis).
o HDL’s pick up excess cholesterol from body cells and return it to the liver.

34
Q

Normal Lipid Values in Blood:

A

o Total cholesterol: Less than 200 mg/dL.
o LDL cholesterol: Less than 130 mg/dL.
o HDL cholesterol: Greater than 40 mg/dL.
o Triglycerides: Less than 150 mg/dL.
o LDL can be estimated from knowing total cholesterol, TG, and HDL:
o LDL = cholesterol minus HDL minus (TG/5).

35
Q

Meds to Lower Blood Lipids:

A

o Drugs that block bile reabsorption:
o Cholestyramine (Questran)/Colestipol (Colestid).
o PCSK-9 inhibitors:
o Increase LDL receptors.
o Drugs that inhibit HMG-CoA reductase (enzyme needed to make cholesterol):
o Statin meds (Lipitor, Zocor, Crestor, Livalo, etc.).
o Nicotinic acid.
o Triglycerides:
o Omega-3 fish oils lower TG.
o EPA (eicosapentaenoic acid).
o DHA (docosahexaenoic acid).
o But ETOH and glucose intolerance increase TG.

36
Q

Protein Metabolism in Fed State:

A

o The liver receives dietary protein in the form of a.a., dipeptides, tripeptides.
o The liver has choices:
o 20 percent of a.a. used to make proteins.
• Proteins liver uses for itself (e.g., carnitine).
• Plasma proteins (name some!).
o 23 percent not taken up by hepatocytes and sent on to other body cells (esp. branch-chain a.a.).
o 57 percent are deaminated, forming alpha-keto acids which are very very versatile.

37
Q

Deamination of Amino Acids:

A

o The amino groups (NH2) turn into toxic ammonia (NH3), which the liver converts to urea (ornithine cycle).
o The alpha-keto acids are versatile:
o Can enter glycolysis—used as fuel.
o Can enter the Kreb’s cycle—used as fuel.
o Can be converted to acetyl-CoA and used to make fatty acids (àTG) or cholesterol.
o Can be converted to GLUCOSE (not all).
o Can be used to make non-essential a.a.

38
Q

Hormones in the Fed State:

A
o	Primary hormone in the FED state is INSULIN.
o	Released by beta cells of pancreas.
o	Stimulus for release of insulin:
o	Vagus nerve.
o	Food hitting duodenum (incretins).
•	GIP.
•	GLP-1.
o	Hyperglycemia (sensed by beta cells).
•	Blood glucose less than 100 mg/dL.
o	Elevated a.a. in the blood.
39
Q

Actions of Insulin:

A

o Insulin targets most body cells
o Insulin is an ANABOLIC HORMONE (helps cells “make stuff”)
o Drives glucose into cells.
o Promotes glycolysis.
o Drives a.a. into cells.
o Drives F.A. into cells.
o Insulin promotes many anabolic pathways:
o Glycogenesis (synthesis of glycogen), Protein synthesis, Lipogenesis (synthesis of TG).
o Insulin decreases many catabolic pathways, including lipolysis and gluconeogenesis.

40
Q

Insulin’s Promotion of Glucose Entry Into Cells:

A

o Insulin interacts with a receptor on cell membrane of target tissues (does not enter the body cell).
o Activates a SIGNAL CASCADE that results in the synthesis of glucose transporters (“taxi’s” that pull glucose into the cell).
o Several types of glucose transporters (GLUT1, GLUT2, GLUT3, GLUT4, etc.).

41
Q

Disorders of the Fed State:

Diabetes Mellitus I and II

A

o Type I DM:
o Usual onset is in childhood.
o Autoimmune disorder, heredity component.
o Beta cells of pancreas are destroyed.
o Insulin levels are non-existent.
o Type II DM:
o Insulin-resistant diabetes—usually make plenty of insulin in the beginning; beta cells may “burn out” in the end.
o Onset in adults, now being seen in kids!
o Several causes possible, at least 10 genes implicated!!!
o Associated with obesity.
o Other Disorders: Metabolic Syndrome, Obesity.

42
Q

Possible Problems with Diabetes Mellitus in Fed State:

A

o Something is wrong with beta cells in pancreas:
o Don’t make enough insulin (beta cell burn out).
o Don’t make insulin in a timely manner (not fast enough).
o Make defective insulin.
o Something is wrong with the insulin receptor on the body cell membrane:
o Receptor is defective or blocked.
o Insufficient numbers of receptors.
o Something is wrong with the signaling cascade !!!!
o Something is wrong with the glucose transporter (taxi):
o Transporter is defective.
o Insufficient numbers of transporters.
o Some other hormone is interfering with the action of insulin:
o Resistin (hormone secreted by adipose tissue)(fat).
o Insulin antagonists are being secreted inappropriately (hGH, glucagon).

43
Q

Summary of Diabetes Mellitus:

A

o Glucose is unavailable to most body cells (exceptions: brain cells, liver, RBC).
o Blood glucose stays very high = hyperglycemia.
o Body tries to compensate by breaking down body fat for cells to use to make ATP.
o If this gets out of hand, then too many 2-carbon fragments turns into ketones.

44
Q

Diabetic Symptoms:

A
o	Type I DM
o	Polyuria (excessive urination).
o	Polydipsia (excessive thirst).
o	Polyphagia (excessive hunger/eating).
o	Type II DM
o	Fatigue.
o	High blood insulin levels (until burnout).
o	Weight gain.
o	Occasionally polyuria and polydipsia.
45
Q

Chronic Problems Associated with Hyperglycemia:

A

o Peripheral neuropathy (pain and decrease sensation).
o Poor wound healing:
o Gangrene.
o Amputation of extremities.
o Microvascular disease:
o Retinal blood vessel disease leads to blindness.
o Kidney disease leads to renal failure.
o Macrovascular disease
o Atherosclerosis leads to CAD leads to MI.
o Atherosclerosis leads to carotid arteries leads to CVA.

46
Q

Metabolic Syndrome:

A

o Constellation of symptoms that increases risk of CVD = Syndrome “X”.
o CDC estimates 34% of US adults have metabolic syndrome.
o Diagnosis based on having at least 3 of following 5 criteria:
o Abnormal abdominal girth (greater than 40” males; greater than 35” female).
o Blood pressure greater than 130/85 mm Hg.
o Fasting blood glucose greater than 110 mg/dL.
o Fasting TG greater than 150 mg/dL.
o Fasting HDL-cholesterol leads to 40 mg/dL.

47
Q

Obesity Increases Risk for:

A
o	Type 2 Diabetes Mellitus.
o	High blood pressure.
o	Cardiovascular disease (MI and CHF).
o	Stroke.
o	Cancers (breast, colon, uterus, prostate).
o	Osteoarthritis and Gout.
o	Sleep apnea.
o	Gall bladder and liver disease.
48
Q

Ratios of Obesity:

A
o	Overweight:
o	Greater than 10 percent over a recommended weight relative to the individual.
o	Body Mass Index (BMI) greater than 25.
o	Obese:
o	Excessive amount of body fat in relation to lean body mass.
o	Body Mass Index (BMI) greater than 30.
o	Body Mass Index (BMI):
o	Multiply your weight in lb. by 700.
o	Divide by your height in inches.
o	Divide by your height in inches again.
49
Q

Metabolism in Post-Absorptive (Unfed) State:

A

o Post-absorptive state = “unfed” state = period when digestive tract is empty and energy sources are supplied by the breakdown of body stores and reserves.
o General Facts:
o Primary goal is to maintain blood glucose levels within homeostatic range (70 to 100 mg/dL).
o Post-absorptive state works at enhancing 2 types of processes:
o 1. Events that make GLUCOSE available to blood:
o Glycogenolysis and Gluconeogenesis.
o 2. Events that SPARE GLUCOSE for organs that need it the most (most body cells can use alternate sources of fuel besides glucose).

50
Q

Events Making Glucose Available in Blood:

A

o Glycogenolysis:
o Liver (100 grams = 400 kcals).
o Skeletal muscle (325 grams, but first must be converted to pyruvic acid to liver).
o Gluconeogenesis:
o Liver (glucose from a.a., glycerol, etc.).
o Lipolysis (only glycerol portion of TG can be converted to glucose) in adipose tissue.
o F.A. can NOT be converted to glucose!
o Catabolism of cellular proteins.
o Kidney (esp. if prolonged unfed state).

51
Q

Events that Spare Glucose:

A

o Lipolysis: TG turns to glycerol + F.A.
o F.A. can be used by most cells to make ATP, leaves glucose for the brain.
o Skeletal muscle cells switch to burning an even greater amt. of F.A. to make ATP.
o Ketosis: Liver oxidizes its stored fats to KETONES and releases ketones into blood for cells to use to make ATP.

52
Q

Ketosis:

A

o If fasting (or a very low-carbohydrate diet) continues for 4 to 5 days, the brain begins to use ketone bodies as well as glucose as its energy source (takes about 2 weeks before the brain can do this efficiently)… in the meantime, tissue protein continues to be broken down to provide the glucose the brain needs.
o Ketones (from excessive beta oxidation) include:
o Aceto-acetic acid.
o Beta-hydroxybutyric acid.
o Acetone (sweet, fruity smell to breath).
o Ketosis creates a low pH situation: acidosis.

53
Q

Neuronal and Hormonal Controls in the Post-Absorptive State:

A

o The major stimulus for regulatory mechanisms is LOW blood glucose.
o Hypothalamus detects low glucose and increases ANS sympathetic output.
o Stimulates adrenal medulla to release Ep and NE.
o Stimulates adipose tissue to mobilize F.A.
o Stimulates pancreatic alpha cells to release glucagon.
o Dropping blood glucose also stimulates ALPHA CELLS of pancreas to release GLUCAGON.
o Targets primarily the liver and adipose tissue.

54
Q

Glucagon:

A

o Targets liver cells:
o Promotes glycogenolysis.
o Stimulates gluconeogenesis.
o Targets adipose tissue:
o Stimulates lipolysis of TG turns into F.A. + glycerol.
o Glycerol travels back to liver for conversion to glucose.

55
Q

Catecholamines:

Ep and NE

A

o Targets liver cells:
o Promotes glycogenolysis and gluconeogenesis.
o Targets adipose tissue:
o Stimulates lipolysis leads to F.A. + glycerol.
o Targets skeletal muscle cells:
o Encourages skeletal muscle to switch to F.A. for ATP production.
o Many other targets!

56
Q

Human Growth Hormone (hGH):

A

o Targets liver cells:
o Stimulates gluconeogenesis.
o Targets adipose tissue:
o Stimulates lipolysis.
o Stimulates protein synthesis by promoting a.a. uptake by cells.
o CLINICAL NOTE: hGH is considered to be an insulin antagonist!

57
Q

Cortisol:

A

o Very Catabolic Hormone.
o Released from the adrenal cortex when blood sugar levels are low.
o Targets liver cells:
o Stimulates gluconeogenesis.
o Targets skeletal muscle cells:
o Stimulates protein catabolism leads to a.a. sent on to liver for gluconeogenesis
o Targets adipose cells:
o Stimulates lipolysis (as long as insulin levels are low).

58
Q

Thermoregulation:

A
o	Hypothalamus = thermostat:
o	Receives signals from peripheral thermoreceptors.
o	Affected by cytokines.
o	Hypothalamic heat-losing center:
o	Cutaneous vasodilation.
o	Sweating.
o	Hypothalamic heat-promoting center:
o	Cutaneous vasoconstriction.
o	Shivering thermogenesis.
o	Non-shivering thermogenesis.
•	Thyroid hormone.
•	Sympathetic nervous system.
59
Q

Disturbances of Thermoregulation:

A
o	Fever:
o	Normal protective mechanism.
o	Increases BMR.
o	Heat cramps:
o	Painful muscle spasms from lyte loss.
o	Heat exhaustion:
o	More severe water and lyte loss.
o	Hypotension, dizziness, vomiting, syncope.
o	Heat stroke (sunstroke):
o	Body gains heat by radiation & conduction, but high humidity prevents dissipation of heat via evaporation of sweat (core temp greater than 40 degrees C).
o	Hypovolemic shock.
o	Often fatal.