Term
| essential amino acids and examples of them |
|
Definition
-amino acids we need, but can't produce
-lysine, methionine, valine, leucine, isoleucine, tryptophan, phenylalanine, and threonine (lys, met, val, leu, ile, try, phe, thr) |
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|
Term
| essential fatty acids and examples of them |
|
Definition
-fatty acids we need to obtain from food
-omega-6 and omega-3 |
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Term
| some examples of water soluble vitamins |
|
Definition
| -Thiamin (B1)
-riboflavin (B2)
-Niacin (B3)
-Pyridoxine (B6)
-Vitamin C |
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|
Term
| the role of water-soluble vitamins |
|
Definition
| coenzymes, widespread effects, cannot be stored in the body |
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Term
|
Definition
| needed to convert pyruvate to acetyl CoA (important for Krebs cycle) |
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|
Term
| the role of Niacin (B3) and riboflavin (B2) |
|
Definition
| needed to make FAD and NAD (used during Krebs cycle for production of ATP) |
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|
Term
| the role of Pyridoxine (B6) |
|
Definition
| needed for amino acid metabolism |
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Term
|
Definition
| antioxidant, helps reduce CV disorders |
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|
Term
| some fat-soluble vitamins |
|
Definition
-Vitamin A
-vitamin D
-vitamin E
-vitamin K |
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|
Term
| role of fat-soluble vitamins |
|
Definition
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Term
|
Definition
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Term
|
Definition
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Term
|
Definition
|
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Term
|
Definition
| blood coagulation/clotting |
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Term
|
Definition
-Molecules with an unpaired electron in their outer orbital
-Highly reactive, oxidizing or reducing other atoms |
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|
Term
| some types of free radicals and examples of them |
|
Definition
| -Reactive oxygen species (ROS) – O2·- and OH·-
-Reactive nitrogen species (RNS) – NO· |
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|
Term
| some organelles that produce free radicals and why they produce them |
|
Definition
-Mitochondria – oxidative phosphorylation, while producing ATP
-Peroxisomes, NADPH oxidase & other enzymes |
|
|
Term
| some functions of free radicals in the body |
|
Definition
-On WBC – destroy bacteria, cause lymphocyte proliferation
-Wound healing – proliferation of fibroblasts
-Vasodilation by NO· |
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|
Term
| what happens to cells when there's too many free radicals? |
|
Definition
|
|
Term
| the cells that do not get oxidatively stressed by free radicals |
|
Definition
-white blood cells
-fibroblasts in the healing process |
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|
Term
| how the oxidative stress occurs |
|
Definition
| Free radicals – highly toxic to cells (OH·-) --> altering the structures of proteins, nucleic acids, lipids, and other molecules --> cell damage --> cell mutation or death |
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|
Term
| health effects of oxidative stress |
|
Definition
| Promotes aging, inflammatory disease, degenerative diseases & malignant growth |
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Term
| some examples of endogenous antioxidant enzymes |
|
Definition
-Superoxide dismutase & superoxide catalase
-Glutathione peroxidase & glutathione reductase |
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|
Term
| some examples of exogenous antioxidants |
|
Definition
-beta-Carotene
-vitamin C, E |
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|
Term
| foods rich in exogenous antioxidants |
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Definition
|
|
Term
| how antioxidants neutralize free radicals |
|
Definition
|
|
Term
| depiction of the important balance that occurs between reactive oxygen species (ROS) production and defense |
|
Definition
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|
Term
| some health problems that can result from having not enough free radicals |
|
Definition
-impaired immune function
-impaired cell proliferation
-other impaired responses |
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|
Term
|
Definition
-fat cells
-adipocytes
-lipocytes |
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|
Term
| PPARγ (peroxisome proliferator activated receptors, subtype gamma) |
|
Definition
| function as transcription factors for activation of genes for differentiation & metabolism |
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|
Term
| how the differentiation of preadipocyte occurs |
|
Definition
| ↑ in circulating fatty acids or prostaglandin (PGJ2) → bind to PPARγ on preadipocytes → ↑ mitosis & differentiation of preadipocytes → ↑ # of adipocytes |
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|
Term
| PPARγ are in the same family as the... |
|
Definition
| R’ for thyroid H, vit A and vit D |
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Term
|
Definition
negative feedback loops to defend maintenance of a certain amount of adipose tissue
A hypothesis that keeps the level of body fat within a narrow range despite considerable variations in dietary fat intake and physical activity
Makes it difficult to lose weight |
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|
Term
| how adipose tissue is an energy source |
|
Definition
-Energy substrate is stored in adipose cells as triacylglycerol (triglycerides, neutral fat)
-The storage and release of neutral fat from adipose cells are hormonally controlled
+Examples – insulin, GH, thyroid H’, adrenal gland H’ |
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|
Term
| how adipose is a hormonal tissue |
|
Definition
-Adipocytes secrete regulatory hormones called adipokines when their PPAR are activated
-Adipokines regulate hunger, metabolism, and insulin sensitivity
-Adipokines include leptin, adiponectin, TNFa, resistin and retinol binding protein-4 (retinol BP4) |
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|
Term
|
Definition
| Hormones (including leptin, adiponectin, TNFα, resistin and retinol binding protein-4 (retinol BP4)) secreted by adipose cells to regulate hunger, metabolism, and insulin sensitivity |
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Term
| how the leptin secreted by adipose tissue affects some of the organs in the body |
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Definition
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|
Term
| how the leptin secreted by adipose tissue functions in energy metabolism |
|
Definition
| ↑ fat tissue → ↑ leptin secretion → ↓ appetite |
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|
Term
| how the leptin secreted by adipose tissue functions in starvation |
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Definition
| ↓ adipose levels --> ↓ leptin levels --> ↓ immune activities |
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|
Term
| how the leptin secreted by adipose tissue functions in reproduction |
|
Definition
-Leptin levels link whether adequate energy reserves are present for normal reproductive function
-Leptin and timing of puberty
-Amenorrhea (cessation of menstrual cycle) of underweight women |
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|
Term
| how obesity leads to type 2 diabetes mellitus (DM) |
|
Definition
Obesity → ↑ secretion of leptin, TNFα, resistin and retinol BP4 from adipocytes → … → ↓ insulin secretion → … → type 2 diabetes mellitus (DM)
obesity → ↓ adiponectin secretion → ↓ muscle insulin sensitivity → … → type 2 DM |
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Term
|
Definition
| insulin-sensitizing, antidiabetic |
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|
Term
| depiction of how leptin is involved in the development of type 2 diabetes mellitus (DM) |
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Definition
|
|
Term
| depiction of how adiponectin is involved in the development of type 2 diabetes mellitus (DM) |
|
Definition
|
|
Term
| how obesity leads to the cells becoming less sensitive to insulin on the way to developing type 2 diabetes mellitus (DM) |
|
Definition
| obesity → ↓ adiponectin secretion → ↓ muscle insulin sensitivity → … → type 2 diabetes mellitus (DM) |
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|
Term
| how the adipocytes behave differently in child and adult obesity |
|
Definition
-Childhood obesity involves increases in both size & number of adipocytes
-Weight gain in adulthood is due mainly to increase in adipocyte size |
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|
Term
| how obesity is often diagnosed |
|
Definition
|
|
Term
|
Definition
| BMI = w/h2
w = weight in kilograms
h = height in meters |
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|
Term
| healthy, overweight, and obese BMI ranges |
|
Definition
-Healthy weight is BMI between 19 – 25
-Overweight – >25 BMI
-obesity – > 30 BMI |
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Term
|
Definition
| BMI has a very positive correlation with cardiovascular disorders; higher BMI positively corresponds to higher risk of cardiovascular disorders |
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|
Term
| the thing in the brain responsible for hunger and regulating eating behavior |
|
Definition
| arcuate nucleus of the hypothalamus |
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Term
|
Definition
| Secretion of neuropeptide Y (NPY) & agouti-related protein (AgRP) --> ↑ hunger --> promote eating |
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Term
|
Definition
| Secretion of melanocyte stimulating hormone (MSH) --> ↓ hunger |
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Term
|
Definition
| ↑ Circulating energy substrates --> ↑ in MSH and ↓ in NPY & ↓ in AgRP secretions --> ↓ appetite |
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|
Term
| neurotransmitters than can increase overeating |
|
Definition
-Endorphin
-norepinephrine |
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|
Term
| neurotransmitters than can decrease overeating |
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Definition
|
|
Term
| depiction of the pathways involving leptin and the hypothalamus that suppress appetite and increase metabolic rate |
|
Definition
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|
Term
|
Definition
|
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Term
|
Definition
| pain-killing effects of endorphin |
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Term
|
Definition
| control outside the blood-brain barrier |
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|
Term
| hormone released by the stomach and what it does |
|
Definition
| Ghrelin (stomach) stimulates hunger via arcuate nucleus |
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|
Term
| hormones released by the small intestine and what they do |
|
Definition
-CCK (SI) promotes satiety
-PYY (SI) responds to caloric content --> ↓ appetite for 12 hrs |
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Term
|
Definition
| a satiety factor, involved in long-term regulation |
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|
Term
| how leptin is a satiety factor |
|
Definition
-Leptin --> ↓ NPY & ↓ AgRP secretions in arcuate N. --> ↓ hunger
-Leptin --> ↑ MSH --> ↓ hunger |
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|
Term
| the pathway by which insulin plays a role in satiety |
|
Definition
| Insulin --> ↓ NPY --> ↓ hunger |
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|
Term
| depiction of how the brain, adipose tissue, pancreas, stomach, and small intestine interact with each other to regulate hunger and appetite |
|
Definition
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|
Term
|
Definition
-contraction of gallbladder, secretion of bile, and then bile acid and bile salt within the bile that can help digestion of fat
-increase and stimulate the secretion of pancreatic digestive enzymes
-promotes satiety, which means the appetite has been reached
-stimulates insulin secretion, increasing the uptake of fatty acids, amino acids, and glucose into the cell |
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|
Term
| the 2 complementary components of metabolism |
|
Definition
-Anabolism (synthesis)
-Catabolism (hydrolysis)
[image] |
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Term
|
Definition
| -Is total rate of body metabolism
-over time, this is equal to the amount of O2 consumed by body/min (over time because anaerobic metabolism is sometimes used) |
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|
Term
| Basal metabolic rate (BMR) |
|
Definition
-Awake, relaxed, 12-14 hr after eating, at comfortable temp
-affected by age (higher in younger people), sex (tends to be higher in males), body surface area (higher in those with larger surface area), thyroid H' |
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|
Term
| relationship between thyroid and Basal metabolic rate (BMR) |
|
Definition
-Hyperthyroidism – high BMR
-Hypothyroidism – low BMR |
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|
Term
| Living cells are maintained by... |
|
Definition
| constant expenditure of energy (ATP) |
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|
Term
|
Definition
glycolysis & Krebs cycle
[image] |
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|
Term
| Fuels used to generate energy include... |
|
Definition
| glucose, fatty acids, amino acids, ketone bodies etc. |
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|
Term
|
Definition
| heat required to elevate 1 cm3 H2O from 14.5-15.5°C |
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|
Term
| energy content of carbohydrates, proteins, and lipids |
|
Definition
-Carbohydrates & proteins – 4 Kcal/gm
-lipids – 9 Kcal/gm |
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|
Term
| Normally brain neurons use ______ as the preferred energy sources (E° substrates) |
|
Definition
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|
Term
| When encountering long-term starvation brain neurons can use ______ for energy |
|
Definition
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|
Term
| The preferred energy sources for resting skeletal muscles |
|
Definition
|
|
Term
| During exercise muscles use... |
|
Definition
|
|
Term
| Which cells can only use glucose as the absolute energy sources? |
|
Definition
|
|
Term
| Why do skeletal muscles prefer to use lipids when at rest and switch to glucose during exercise? |
|
Definition
| because at rest, they spare the glucose for use by the brain |
|
|
Term
| why red blood cells can only use glucose for energy |
|
Definition
because they don't have mitochondria, and therefore no Krebs cycle
-they can only do glycolysis |
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|
Term
|
Definition
-within 4 hr period after eating
-Absorption of abundant energy substrates (anabolic) |
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|
Term
| some anabolic processes that occur during the absorptive state |
|
Definition
-Glucose in excess → ↑ glycogenesis in liver (main) & skeletal muscles
+If excess exists after full glycogenesis → ↑ lipogenesis
-Fatty acids in excess → ↑ lipogenesis
-Amino acids in excess → ↑ protein synthesis |
|
|
Term
| why too much sugar results in obesity |
|
Definition
| because if excess exists after full glycogenesis → ↑ lipogenesis |
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|
Term
|
Definition
–fasting state, > 4 hr after the meal
-Use of the stored energy substrates for energy (catabolic) |
|
|
Term
| some catabolic processes that occur during the postabsorptive state |
|
Definition
| ↑ Glycogenolysis, lipolysis & protein degradation |
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|
Term
| some energy-producing processes that occur during short-term to long-term starvation states |
|
Definition
-gluconeogenesis
-ketogenesis |
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Term
|
Definition
| formation of glucose from non-carbohydrates (amino acids, glycerol, lactate etc.) |
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|
Term
|
Definition
| formation of ketone bodies from lipids |
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Term
|
Definition
| Conversion of glucose into two molecules of pyruvic acid |
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Term
|
Definition
| The production of glycogen, mostly in skeletal muscles and the liver |
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Term
|
Definition
| Hydrolysis (breakdown) of glycogen; yields glucose 6-phosphate for glycolysis, or (in the liver only) free glucose that can be secreted into the blood |
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Term
|
Definition
| The production of glucose from noncarbohydrate molecules, including lactic acid and amino acids, primarily in the liver |
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Term
|
Definition
| The formation of triglycerides (fat), primarily in adipose tissue |
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|
Term
|
Definition
| Hydrolysis (breakdown) of triglycerides, primarily in adipose tissue |
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|
Term
|
Definition
| The formation of ketone bodies, which are four-carbon-long organic acids, from fatty acids; occurs in the liver |
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|
Term
| specific disease in which the patient often has ketogenesis |
|
Definition
|
|
Term
| The body's transiion between anabolism and catabolism is mainly regulated by... |
|
Definition
|
|
Term
| some hormone changes in absorptive and postabsorptive states |
|
Definition
-Absorptive state – ↑ insulin secretion
-postabsorptive state – ↑ glucagon secretion |
|
|
Term
| diagram showing how the balance between anabolism and catabolism is maintained |
|
Definition
|
|
Term
| some hormones involved in maintaining the balance between anabolism and catabolism |
|
Definition
| antagonistic effects of insulin, glucagon, GH, T3, cortisol, and Epi |
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|
Term
| some hormones that regulate metabolism under certain physiological conditions |
|
Definition
-Adrenal hormones (H) – stress
-Thyroid H – basal metabolic rate & growth
-GH – growth & maintenance |
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|
Term
| why insulin secretion increases in the absorptive state |
|
Definition
overabundant of E° substrates (glucose, amino acids & fatty acids) --> ↑ insulin secretion
-Overall strategy – ↓ blood levels of E° substrates by storing in tissues |
|
|
Term
| some things that are caused by increased insulin levels |
|
Definition
When blood [insulin] increases --> ↑ anabolism and ↓ catabolism
-↑ Insertion of glucose transporters 4 on skeletal, cardiac muscles & fat tissue
+↑ Cellular uptake of glucose
-↑ Glycogenesis – ↑ entry of glucose into liver & skeletal muscle cells --> ↑ glycogen storage
-↑ Lipogenesis – ↑ neutral fat in adipose cells
-↑ Cellular uptake of amino acids --> ↑ proteins synthesis |
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|
Term
| how insulin and glucagon interact with liver cells |
|
Definition
|
|
Term
| how insulin interacts with adipose cells |
|
Definition
|
|
Term
| why glucagon levels increase in the postabsorptive state |
|
Definition
Postabsorptive state --> ↓ blood levels of glucose & fatty acids
-Overall strategy – to maintain blood glucose & fatty acids |
|
|
Term
| depiction of what happens how the adipose, liver, and skeletal muscles interact with each other during fasting |
|
Definition
|
|
Term
| some things that happen when glucagon levels increase |
|
Definition
-↑ glucagon --> ↑ Glycogenolysis in the liver --> ↑ blood glucose levels
-Also, ↑ glucagon --> ↑ lipolysis --> ↑ blood fatty acid levels (skeletal muscle, heart, liver, & kidneys use fatty acids as major source of fuel) |
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|
Term
| what higher glucagon levels lead to during mid- to long-term starvation |
|
Definition
| ↑ Gluconeogenesis & ketogenesis |
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|
Term
| Normal fasting [glucose] levels |
|
Definition
|
|
Term
| how blood glucose levels are maintained during the absorptive state |
|
Definition
Absorptive state – ↑ blood [glucose] (main effect) or ↑ blood [amino acids] --> ↑ insulin secretion
-↑ Blood [glucose] --> glucose binds to glucose transporter GLUT2 in β cells (GLUT2 is not insulin-regulated) --> ↑ insulin secretion --> glucose enters cells
-Insulin and glucagon normally prevent levels from rising above 170 mg/dl or falling below 50 mg/dl |
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|
Term
| how blood glucose levels are maintained during the postabsorptive state |
|
Definition
Post-absorptive or stressful state – ↑ glucagon
-↑ Glucagon secretion occurs only when ↓ blood [glucose] |
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|
Term
| meals that increase levels of both insulin and glucagon anh why they do it |
|
Definition
meals high in protein and low in carbohydrates
-this is because amino acids stimulate insulin production and low carbs stimulate glucagon production
-a perfect example of this is the Atkins diet |
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|
Term
| why hypoglycemia can cause neurological problems |
|
Definition
| because neurons rely mainly on glucose |
|
|
Term
| the effect of the autonomic nervous system on blood glucose levels |
|
Definition
-Sympathetic effect - “fight or flight”, enhances glucagon secretion, stress hyperglycemia
-Parasympathetic effect - “rest and repair”, “+” insulin |
|
|
Term
| the 3 hormones that regulate insulin and glucagon secretion and how they do it |
|
Definition
-GIP
-CCK
-GLP-1
-Glucose in gut --> ↑ GIP (glucose-dep. insulinotropic peptide) secretion --> ↑ insulin secretion, ↓ gastric motility
+Glucose ingestion vs. i.v. glucose injection
-CCK (cholecystokinin) --> ↑ insulin secretion, ↑ secretion of bile and pancreatic digestive enzymes
-↑ Blood glucose, amino acids, fatty acids --> ↑ GLP-1 (glucagon-like peptide, incretin) --> ↑↑↑ insulin, β cell proliferation & ↓ appetite (potent anti-hyperglycemic) |
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|
Term
| how higher glucagon levels lead to stimulation of sympathetic division of the ANS |
|
Definition
| higher glucagon --> glycogen breakdown --> higher blood glucose levels stimulation of sympathetic division of ANS for "fight-or-flight" reaction |
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|
Term
| why ingesting sugar causes more insulin release than injecting sugar |
|
Definition
because ingesting it, there's contact with the epithelial cells of the small intestine, leading to more secretion of insulin
Glucose in gut --> ↑ GIP (glucose-dep. insulinotropic peptide, or gastric inhibitory peptide) secretion --> ↑ insulin secretion, ↓ gastric motility |
|
|
Term
| glucagon-like protein 1 (GLP-1) |
|
Definition
-stimulates insulin secretion and decreases glucagon secretion
-this is a potent anti-hyperglycemic hormone
-↑ Blood glucose, amino acids, fatty acids --> ↑ GLP-1 (glucagon-like peptide, incretin) --> ↑↑↑ insulin, β cell proliferation & ↓ appetite (potent anti-hyperglycemic) |
|
|
Term
|
Definition
| chronic ↑ in blood [glucose] |
|
|
Term
| Type 1 Diabetes mellitus (DM) |
|
Definition
juvenile-onset, insulin-dependent (ID) DM
-Occurs mainly at juvenile age, ~5% of DM patients |
|
|
Term
| how Type 1 Diabetes mellitus (DM) is an autoimmune disease |
|
Definition
-the virus that causes it resembles glutamate dacarboxylase
-as a result, killer T cells target glutamate decarboxylase in Beta cells → Beta cells destroyed, Alpha cells active → ↓ insulin |
|
|
Term
| in type 1 diabetes, hyperglycemia is due to... |
|
Definition
-Lack of insulin → glucose cannot enter the adipose cells
-↑ Glucagon/insulin ratio → ↑ glycogenolysis in liver → ↑ glucose exit into blood from liver → hyperglycemia
-Lack of insulin → rate of lipolysis > rate of lipogenesis → ↑ fatty acids in blood
-Fatty acids converted to ketone bodies → hyperketonemia → ketoacidosis → coma |
|
|
Term
| why someone with type 1 diabetes may need to drink lots of water |
|
Definition
because type 1 diabetes causes Osmotic diuresis
-Osmotic diuresis → glucosuria, dehydration |
|
|
Term
|
Definition
increase in blood volume caused by osmotic pressure
-often seen in type 1 diabetes |
|
|
Term
| why people with type 1 diabetes may have larger appetites |
|
Definition
| because glucose and fatty acids can't enter the cells, due to lack of insulin |
|
|
Term
| some details about Type 2 Diabetes Mellitus (DM) |
|
Definition
-aka non-insulin-dependent (NIDDM)
-Account for 95% of DM patients
-Insulin resistance – cells fail to respond to insulin actions
-Blood [insulin] may be high or normal until late stage
-Slow to develop, genetic factors play a role
-Occurs mostly in mid-age people who are overweight |
|
|
Term
| how insulin resistance leads to type 2 diabetes |
|
Definition
When fat and muscle cells fail to respond adequately to circulating insulin, blood glucose levels rise
-glucose and fatty acids can't enter cells, due to insulin resistance |
|
|
Term
| treatment for type 2 diabetes |
|
Definition
Treatment – change in lifestyle:
-Increase exercise → ↑ GLUT-4 in the skeletal muscle cells (makes them more responsive to insulin)
-Weight reduction – ↑ fiber in diet, ↓ saturated fat |
|
|
Term
| the primary cause of type 2 diabetes |
|
Definition
|
|
Term
| hypothesis for how increased dietary levels of polyunsaturated fatty acids can treat type 2 diabetes |
|
Definition
| ↑ polyunsaturated fatty acids → ↑ cell membrane fluidity → ↑ insulin R’ # → ↑ affinity of insulin to its receptors → ↓ insulin resistance |
|
|
Term
| oral glucose tolerance test |
|
Definition
one way to tell whether or not a patient has diabetes
-A person drinks a glucose solution and blood samples are taken periodically
-Normal person’s rise in blood [glucose] after drinking solution is reversed to normal in 2 hrs
-measures...
+Ability of Beta cells to secrete insulin (insulin secretion)
+Ability of insulin to lower blood glucose (insulin-resistance)
[image] |
|
|
Term
| indicator of diabetes after the oral glucose tolerance test |
|
Definition
Blood [glucose] levels in DM patients remain > 200 mg/dl 2 hr following glucose ingestion
[image] |
|
|
Term
|
Definition
-Symptoms of hypoglycemia
-Insulin injections → insulin shock
[image] |
|
|
Term
| the oral glucose tolerance test measures... |
|
Definition
-Ability of Beta cells to secrete insulin (insulin secretion)
-Ability of insulin to lower blood glucose (insulin-resistance)
[image] |
|
|
Term
| adrenal medulla secretes... |
|
Definition
-epinephrine (E)
-norepinephrine (NE) |
|
|
Term
| effects of the epinephrine (E) and norepinephrine (NE) secreted by the adrenal medulla |
|
Definition
-Fight or flight (sympathetic, short-term stress) --> need glucose for CNS & skeletal muscles
-epinephrine ↑ Glycogenolysis --> hyperglycemia
-epinephrine ↑ Lipolysis, converting fat into fatty acids – glucagon-like effects
-Second messenger – cAMP (similar to glucagon) |
|
|
Term
| adrenal cortex secretes... |
|
Definition
| glucocorticoids (e.g. cortisol) |
|
|
Term
| effects of the glucocorticoids (e.g. cortisol) secreted by the adrenal cortex |
|
Definition
-Long-term stress --> ↑ hypothalamic CRH --> ↑ pituitary ACTH --> ↑ glucocorticoids secretion
-↑ Glucagon secretion --> glycogenolysis --> hyperglycemia
-↑ Lipolysis, ketogenesis & hyperketoemia
-↑ Protein breakdown, gluconeogenesis --> hyperglycemia & general weakness |
|
|
Term
| what the word glucocorticoid means |
|
Definition
steroid hormone secreted by the adrenal cortex for glucose metabolism
-gluco: glucose
-corti: adrenal cortex
-coid: steroid |
|
|
Term
| the stress associated with glucocorticoids |
|
Definition
|
|
Term
|
Definition
| too much ketone bodies in the blood |
|
|
Term
| the 2 thyroid hormones released by the thyroid gland |
|
Definition
| Main form is T4 (thyroxine), active form is T3 |
|
|
Term
| some effects of thyroid hormone |
|
Definition
-Basal metabolic rate (BMR)
-Calorigenic effects (↑ metabolic heat) and cold adaptation |
|
|
Term
|
Definition
|
|
Term
| role of T4 in growth and development |
|
Definition
-Protein synthesis
-Growth of skeleton
-Contributes to proper growth and development of CNS – prenatal to 6 months after birth |
|
|
Term
| symptoms of Hyperthyroidism |
|
Definition
| high BMR, weight loss, nervousness, irritability, intolerance to heat |
|
|
Term
| symptoms of Hypothyroidism |
|
Definition
| cretinism, myxedema, lethargy, weight gain, increased sleep, lower b.t., coarse skin, slow pulse and reflex, depression |
|
|
Term
|
Definition
| mental retardation during fetal or neonatal stage caused by hypothyroidism |
|
|
Term
|
Definition
| when hypothyroidism causes edema by attracting mucoproteins into the extracellular fluid from the blood plasma into interstitial fluid |
|
|
Term
| diagram of what growth hormone influences and what that leads to |
|
Definition
|
|
Term
| secretion of growth hormone (GH) controlled by... |
|
Definition
| growth hormone inhibiting hormone (GHIH) and growth hormone releasing hormone (GHRH), both released by the hypothalamus |
|
|
Term
| growth hormone inhibiting hormone (GHIH) and growth hormone releasing hormone (GHRH) are released by the... |
|
Definition
|
|
Term
| growth hormone released by the... |
|
Definition
|
|
Term
| indirect effects of growth hormone (somatotropin) |
|
Definition
(↑ body growth) – effects on bone & muscles, mediated by IGF 1
[image] |
|
|
Term
| direct effects of growth hormone (somatotropin) |
|
Definition
-Anabolic effects – ↑ protein synthesis, ↑ cell uptake of amino acids
-Catabolic effects – ↑ lipolysis, ↑ blood [fatty acids], ↑ use of fatty acids
[image] |
|
|
Term
| Diabetogenic effect of growth hormone (somatotropin) |
|
Definition
↓ glycolysis rate, ↓ glucose utilization --> hyperglycemia
[image] |
|
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Term
| what the word somatotropin means |
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Definition
A substance stimulates the growth of body
-"In" is a substance
-"Trop" is the growth of
-"Somato" means body |
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Term
| indirect effect of growth hormone (somatotropin) mediated by... |
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Definition
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Term
| In childhood, GH overproduction leads to... |
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Definition
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Term
| In childhood, GH underproduction leads to... |
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Definition
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Term
| In adulthood, GH overproduction leads to... |
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Definition
| acromegaly (jaw elongation; deformities in face, hands & feet bones) |
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Term
| Importance of plasma Ca2+ in the body |
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Definition
| Bone structure, muscle contraction, neurotransmission, second messenger, membrane permeability, maintaining membrane potential |
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Term
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Definition
| enhanced nerve excitability --> muscle spasm (tetanus) |
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Term
| some sources of of plasma Ca2+ |
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Definition
| -Bone deposition and resorption
+Skeleton also serves as a storage of Ca2+
+Osteoblasts for bone deposition (collagen + Ca2+) vs. osteoclasts for bone resorption
-Intestinal absorption and urinary excretion |
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Term
| depiction of how the osteoclast degrades bone |
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Definition
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Term
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Definition
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Term
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Definition
-for bone deposition
-It will deposit collagen, and collagen is a network or meshwork, and then calcium and phosphate will deposit to form the bone structure |
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Term
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Definition
-for bone resorption
-takes calcium away from the bone |
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Term
| Parathyroid hormone (PTH) |
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Definition
| -polypeptide hormone secreted from parathyroid gland
-increases blood Ca2+
-Single most important hormone in the control of blood [Ca2+]
-Stimulating bone resorption of Ca2+
-Stimulating renal reabsorption of Ca2+
-Inhibiting renal reabsorption of PO43-
-Promoting formation of (OH)2 Vit D3 |
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Term
| Over-secretion of PTH leads to... |
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Definition
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Term
| depiction of where the parathyroid glands are |
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Definition
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Term
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Definition
-attached to, but not part of, thyroid gland
-secretes parathyroid hormone, which is a polypeptide hormone |
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Term
| how parathyroid hormone (PTH) increases blood Ca2+ |
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Definition
| -Stimulating bone resorption of Ca2+
-Stimulating renal reabsorption of Ca2+
-Inhibiting renal reabsorption of PO43-
-Promoting formation of dihydroxyl ((OH)2) Vit D3 |
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Term
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Definition
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Term
| the bioactive form of vitamin D3 |
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Definition
| 1,25-dihydroxy-vitamin D3 |
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Term
| the organs that form 1,25-dihydroxy-vitamin D3 |
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Definition
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Term
| how 1,25-dihydroxy-vitamin D3 helps regulate Ca2+ absorption |
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Definition
| stimulates...
-Intestinal absorption of Ca2+
-Bone resorption of Ca2+
-Renal re-absorption of Ca2+ |
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Term
| depiction of the sunlight-dependent pathway that forms 1,25-dihydroxy-vitamin D3 |
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Definition
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Term
| the negative feedback loop 1,25-dihydroxy-vitamin D3 is involved in |
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Definition
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Term
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Definition
| -a peptide hormone secreted by parafollicular (C) cells in the thyroid gland (not parathyroid)
-lowers plasma Ca2+ by ↓ bone resorption (↓ osteoclasts activity) and ↓ renal reabsorption (↑ urinary excretion of Ca2+) |
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Term
| how calcitonin lowers plasma Ca2+ |
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Definition
-↓ Bone resorption – ↓ osteoclast activity
-↓ Renal re-absorption – ↑ urinary excretion of Ca++ |
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Term
| the negative feedback loop calcitonin is in |
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Definition
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Term
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Definition
small cells in the thyroid gland that secrete calcitonin and are just outside the follicles
[image] |
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Term
| a treatment for osteoporosis that uses calcitonin |
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Definition
| nasal spray that gets absorbed through the mucosal layer of the respiratory tract |
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Term
| how the thyroid responds to high Ca levels |
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Definition
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Term
| how estrogen regulates bone growth |
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Definition
-Causes sealing (ossifying) of epiphyseal disc (cartilaginous growth plates) --> stops growth
-Is necessary for proper bone mineralization & prevention of osteoporosis
-Stimulates osteoblast activity & suppresses formation of osteoclasts
[image] |
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