Olson Flashcards

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Olson Flashcards
2011-04-03 18:24:00
Olson Cards

Olson Flashcards
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  1. This refers to the enzyme-catalyzed processes in the body that metabolize macronutrients (carbohydrates, fats, and proteins)
    Intermediary Metabolism
  2. These are reactions that capture chemical energy in the form of ATP. They are typically oxidative and use NAD or FAD as a coenzyme factor.
    Catabolic Pathways
  3. Catabolic pathways are typically ________ and use ____ or _____ as a coenzyme factor
    • Oxidative
    • NAD or FAD
  4. These combine small molecules to make complex molecules. These reactions require energy. They are generally reductive and use NADPH as an electron donor.
    Anabolic Pathways
  5. Anabolic pathways are generally ________ and use ______ as an electron donor.
    • Reductive
    • NADPH
  6. This organ transports ions to maintain membrane potential; integrates inputs from the body and surroundings; and sends signals to other organs
  7. This organ secretes insulin and glucagon in response to changes in blood glucose concentration
  8. This organ processes fats, carbohydrates, and proteins from the diet; synthesizes and distributes lipids, ketone bodies, and glucose for other tissues; and converts excess nitrogen to urea
  9. This organ carries nutrients from the intestine to the liver
    Portal Vein
  10. This organ absorbs nutrients from the diet, moves them into blood or the lymphatic system
    Small Intestine
  11. This organ uses ATP to do mechanical work
    Skeletal Muscle
  12. This organ synthesizes, stores, and mobilizes triacylglycerols
    Adipose Tissue
  13. This organ carries lipids from the intestine to the liver
    Lymphatic System
  14. What are the macronutrients from the diet?
    Carbohydrates, Fats, and Proteins
  15. Within the Glycolysis Pathway, Glucose is converted to what three molecules? Where does this occur?
    • Pyruvate + NADH + H
    • Cytosol
  16. Within the Pyruvate Dehydrogenase Complex Pathway, Pyruvate is converted to what 3 molecules? Where does this occur?
    • Acetyl CoA + NADH + H
    • Mitochondria
  17. Within the Beta-Oxidation Pathway, Fatty Acid is converted to what four molecules? Where does this occur?
    • Acetyl CoA + FADH2 + NADH + H
    • Mitochondria
  18. The oxidation of Acetyl CoA results in reduced ______ and ______. These compounds carry the electrons derived from oxidizing Acetyl CoA to flow through the electron transport chain to drive the synthesis of ATP
    • NADH
    • FADH2
  19. Acetyl CoA is usually oxidized through what pathway?
    Krebs Cycle
  20. Acetyl CoA is synthesized into other energy containing compounds for storage or distribution to other tissues. During the _____ state:
    Acetyl CoA + Oxaloacetate are converted to Fatty Acids
    This occurs in the Cytosol
    Fed State
  21. Acetyl CoA is synthesized into other energy containing compounds for storage or distribution to other tissues. During the _____ state:
    Acetyl CoA is converted to Ketones
    This occurs in the Mitochondria
    Fasted State
  22. What two pathways produce free glucose?
    • Gluconeogenesis
    • Glycogenolysis
  23. Name the Pathway:
    Amino Acids, Glycerol, or Lactate is converted to Glucose
  24. Name the Pathway:
    Glycogen is converted to Glucose
  25. This cycle requires metabolic adaptations and changes in the specific functions of internal organs
    Feeding/Fasting Cycle
  26. The feeding cycle is under the control of _______, and the fasting cycle is under the control of _______ and ________. These hormones have antagonistic effects.
    • Insulin
    • Glucagon & Epinephrine
  27. Does the hormone Insulin in the feeding cycle increase or decrease Glycogenesis, Gluconeogenesis, Ketogenesis, and Lipolysis?
  28. Do the hormones Glucagon and Epinephrine in the fasting cycle increase or decrease Glycogenesis, Gluconeogenesis, Ketogenesis, and Lipolysis?
  29. This is a polypeptide hormone that is synthesized as a preprohormone that is heavily processed prior to secretion.
  30. This hormone is synthesized and secreted from a regulated exocytosis pathway in the beta-cells portion of the islets that make up the endocrine pancreas
  31. After consuming a meal, glucose levels in the portal circulation increase or decrease?
  32. Following a meal, blood levels of glucose (increase/decrease)? Insulin (increase/decrease)? Glucagon (increase/decrease)?
    • Glucose = Increase
    • Insulin = Increase
    • Glucagon = Decrease
  33. The insulin receptor is a ______ ______ enzyme that is activated when it binds to insulin. This sets off a cascade of intracellular phosphorylation events that change the function of the target cell.
    Tyrosine Kinase
  34. The activated insulin receptor activates what four functions?
    • Glucose Uptake
    • Glycogen Synthesis
    • Protein Synthesis
    • Fat Synthesis
  35. The activated insulin receptor inhibits what three pathways?
    • Gluconeogenesis
    • Glycogenolysis
    • Lipolysis
  36. What are the counterregulatory hormones (2)? These are the hormones that oppose the actions of insulin, and function in the fasting state when insulin levels are low.
    • Glucagon
    • Epinephrine
  37. The specific cell surface receptors of glucagon and epinephrine are what type? Activation of these receptors increases intracellular levels of _______, a second messenger. This changes the function of the target cell.
    • G-Protein Coupled Receptors
    • cAMP
  38. Secretion of glucagon from ____ cells is stimulated by _________, and inhibited by _______ and _______.
    • Alpha
    • Epinephrine
    • Glucose & Insulin
  39. Epinephrine is secreted from the ______ _______ in response to _________ under the action of the sympathetic nervous system.
    • Adrenal Medulla
    • Hypoglycemia
  40. Glucagon and epinephrine increase the biological actions of what 5 things? What does it decrease the biological actions of?
    • Glycogenolysis, Gluconeogenesis, Lipolysis, Ketogenesis, & Uptake of Amino Acids
    • Glycogenesis
  41. This state is the 2-4 hour period following ingestion of a meal. Nutrients are being digested in the intestines, and delivered to the body.
    Absorptive or Fed State
  42. In the Absorptive or Fed State, is the metabolism anabolic or catabolic?
    Anabolic, and geared towards storage
  43. What is the dominant hormone that regulates the absorptive or fed state?
    Insulin: it is secreted from beta cells of the endocrine portion of the pancreas in response to rising glucose and amino acid levels in the blood in the portal circulation
  44. What is the function of the intestine during the absorptive or fed state?
    Absorbing nutrients and synthesizing chlyomicrons
  45. What is the function of the liver during the absorptive or fed state?
    Taking up carbohydrate from the portal circulation and using it for glycolysis, glycogen synthesis, and de novo fatty acid synthesis. Chylomicrons are taken up by the liver for recycling of remaining lipid cargo
  46. In the fed state, the liver is a _______ organ
  47. When Glucose enters the liver during the fed state, it can be shuttled into the hexosmono-phosphate shunt pathway (HMP). What does this pathway produce?
    • Ribose
    • NADPH
  48. What is the function of adipose tissue during the absorptive or fed state?
    Taking up dietary fat packaged in chlyomicrons and some glucose from the blood. Lipid storage is the most important task for adipose tissue after a meal
  49. How does Glucose enter the Adipocyte?
    GLUT 4 Transporter
  50. Insulin promotes storage of fat in what 3 ways?
    • Increases lipoprotein lipase (breaks down triacylglycerol)
    • Increases fatty acid transport proteins
    • Inhibits hormone synthesis lipase
  51. What is the function of skeletal muscle during the absorptive or fed state?
    Taking up glucose and using it for glycolysis and glycogen synthesis. Actively taking up amino acids and synthesizing new proteins to repair and rejuvenate the muscle fibers.
  52. What is the most important fuel for resting muscle in the fed state? What is a secondary energy substrate?
    • Glucose
    • Lipid
  53. Muscle is able to remove what molecule from branched-chain amino acids?
  54. What is de novo fatty acid synthesis, or de novo lipogenesis?
    Synthesis of fatty acids from non-lipid derived acetyl CoA
  55. What hormone promotes lipogenesis through phosphorylation cascades and increasing the rates of synthesis of transcription factors that regulate lipogenic enzmes?
  56. What two organs are responsible for lipogenesis?
    • Liver
    • Adipose Tissue
  57. What is the primary source for de novo fatty acid synthesis?
  58. This organ synthesizes new fatty acids for esterification into triacylglycerol, and packaging as VLDL particles for distribution throughout the body. This process is driven by the availability of excess acetyl CoA and NADPH substrates required for the reaction
  59. This organ synthesizes new fatty acids from glucose taken up after a meal. The triacylglycerol is stored in the adipose tissue awaiting mobilization during periods of fasting.
    Adipose Tissue
  60. What is the primary source of glycerol phosphate backbones for esterification of new fatty acids into triacylglycerol
    Glycolysis in Adipose Tissue
  61. When does de novo fatty acid synthesis occur in the liver and adipose tissue?
    When the concentration of acetyl CoA and NADPH in the cytoplasm is high
  62. Cytosolic acetyl CoA comes from acetyl CoA that is produced in the ____________ as a result of glycolysis. The acetyl CoA is converted to _______, which is able to either flux through the Krebs cycle, or cross the inner mitochondrial membrane to enter the cytosol.
    • Inner Mitochondrial Matrix
    • Citrate
  63. Within the mitochondrial matrix,
    Oxaloacetate + Acetyl CoA ---> Citrate

    The citrate can then cross the inner mitochondrial membrane.
    What enzyme catalyzes this reaction? What is given off as a by-product?
    • Citrate Synthase
    • CoA
  64. After crossing through the inner mitochondrial matrix,
    Citrate + CoA --> Oxaloacetate + Acetyl CoA

    This is how we get acetyl CoA into the cytosol, since there are no CoA carriers.
    What enzyme catalyzes this reaction? What molecule is required for this reaction to take place?
    • ATP-Citrate Lyase
    • ATP
  65. What is the major pathway for getting NADPH into the cytosol? How many NADPH molecules are produced for every glucose that enters this pathway? What is the major source?
    • Hexose MonoPhosphate Pathway (HMP)
    • 2
    • Glucose-6-phosphate
  66. Why is it so important to get Acetyl CoA and NADPH into the cytosol?
    They are the main building blocks for new fatty acid synthesis
  67. What enzyme acts on Oxaloacetate that is produced as a result of citrate lyase in the cytosol? This is a minor source for generation of what?
    • Malic Enzyme
    • NADPH
  68. What are the two uses of Malonyl CoA?
    • Fatty Acid Synthesis
    • Potent Inhibitor of Fatty Acid Oxidation
  69. The first important regulated step in the synthesis of Malonyl CoA is the synthesis of Malonyl CoA from Acetyl CoA in the cytoplasm. What enyzme catalyzes this reaction? What are two methods by which this reaction is regulated?
    • Acetyl CoA Carboxylase (ACC) Complex
    • Phosphorylation/Dephosphorylation Cascades & Allosteric Assembly
  70. The synthesis of Palmitate is a multi-step reaction that is catalyzed by what complex? This reaction begins with 1 molecule of Acetyl CoA as a primer and 1 molecule of Malonyl CoA to elongate the chain. A series of reactions are required to produce a reduced hydrocarbon chain. How many times is the cycle repreated to produce Palmitic Acid, a ___ C Saturated Fatty Acid?
    • Fatty Acid Synthase (FAS) Complex
    • 7
    • 16
  71. What are the three important roles Glucose metabolism plays in Palmitate Synthesis?
    • Glycolysis and Pyruvate oxidation to acetyl CoA
    • Production of Oxaloacetate
    • Production of NADPH
  72. To synthesize the newly synthesized fatty acids into triacylglycerol, ________ ________ backbones are required. What are the two sources of this in the liver? How is it generated by adipose tissue?
    • Glycerol Phosphate
    • Partial flux through glycolysis & direct phosphorylation of glycerol by the enzyme glycerol kinase
    • Partial flux through glycolysis
  73. In order to synthesize triacylglycerol from new fatty acids, the fatty acids must be activated to ___________, and these are esterified to ____________ in a 4 step reaction.
    • Fatty-Acyl CoA
    • Glycerol Phosphate
  74. In the synthesis of triacylglycerol from new fatty acids, step one in the reaction involves the conversion:
    Glycerol Phosphate ---> Lysophosphatidic Acid

    What enzyme catalyzes this reaction? What is required for this reaction to take place, and what is given off as a by-product?
    • Acyltransferase
    • Fatty-acyl CoA --> CoA
  75. In the synthesis of triacylglycerol from new fatty acids, step two in the reaction is:
    Lysophosphatidic Acid --> Phosphatidic Acid (DAG phosphate)

    What enzyme catalyzes this reaction? What is required for this reaction to take place, and what is given off as a by-product? What is Phosphatidic Acid a pre-cursor of?
    • Acyltransferase
    • Fatty-acyl CoA --> CoA
    • Plasma membrane pre-cursor -- if needed, doesn't continue in triacylglycerol synthesis
  76. In the synthesis of triacylglycerol from new fatty acids, step three in the reaction is:
    Phosphatidic Acid (DAG phosphate --> Diacylglycerol

    What enzyme catalyzes this reaction? What is required for this reaction to take place, and what is given off as a by-product?
    • Phosphatase
    • H2O
    • Pi
  77. In the synthesis of triacylglycerol from new fatty acids, step four in the reaction is:
    Diacylglycerol ---> Triacylglycerol

    What enzyme catalyzes this reaction? What is required for this reaction to take place, and what is given off as a by-product?
    • Acyltransferase
    • Fatty-acyl CoA --> CoA
  78. Fat stores are sufficient to meet energy needs for about ____ months
  79. What do the hormones of fasting activate? What are the three hormones of fasting?
    • Catabolism, leading to the breakdown of protein, triacylglycerol, and glycogen
    • Glucagon, Epinephrine, and Cortisol
  80. What hormone is secreted from the pancreas in response to lowering insulin levels? It activates a G-protein coupled receptor, and results in an increase in _______, the second messenger that is responsible for changing liver function to support fasting metabolism?
    • Glucagon
    • cAMP
  81. What hormone is secreted from adrenal glands and activates the adrenergic receptors on most tissues, including heart, skeletal muscle, adipose tissue, and liver? The adrenergic receptors are also G-protein coupled receptors, and results in the activation of ______.
    • Epinephrine
    • cAMP
  82. What hormone is secreted from adrenal glands and activates the glucocorticoid receptor, which is a member of the Nuclear Steroid Receptor superfamily? The activated glucocorticoid receptor regulates the transcription of proteins and enzymes that regulate fasting metabolism. The secretion of this hormone is higher as "stress" is increased. It is secreted slowly, and induces longer term changes.
  83. An activated ________ receptor regulates the transcription of proteins and enzymes that regulate fasting metabolism
  84. During fasting metabolism, the liver becomes a ________ organ that secretes _______. It also oxidizes ______ _______ and produces _________. Both of these products secreted by the liver are used by other tissues for energy metabolism and synthesis of ATP.
    • Glucogenic
    • Glucose
    • Fatty Acids
    • Ketones
  85. During fasting metabolism, Glucose exits the liver through what receptor type?
    GLUT 2
  86. During fasting metabolism, the amino acids, glycerol, and lactate that enter the liver enter into ___________, or energy metabolism.
  87. During fasting metabolism, adipose tissue is under control of what hormone? This hormone activates the Hormone Sensitive Lipase, which cleaves triacylglycerol, allowing free fatty acids and glycerol to be secreted from adipose stores.
  88. Hormone Sensitive Lipase, involved in adipose tissue during fasting metabolism, is activated by ___________ and deactivated by _________.
    • Phosphorylation
    • Dephosphorylation
  89. An increase in insulin levels during fasting metabolism can degrade ______ and activate phosphates that make ________ ________ ________ active.
    • cAMP
    • Hormone Sensitive Lipase
  90. Resting skeletal muscle and heart rely heavily on ______ ________ ________ during starvation.
    Fatty Acid Oxidation
  91. The normal substrate for the brain is glucose. As fasting proceeds, the brain adapts to using ______, and will function quite well using this.
  92. What is an important pathway for driving ATP synthesis in liver, skeletal muscle and heart under fasting conditions?
    Beta-Oxidation of Fatty Acids
  93. What are the two ways in which free fatty acids are delivered to the liver, skeletal muscle and heart under fasting conditions?
    • Nonesterified fatty acids released from adipose tissue
    • Lipoprotein lipase action on lipoprotein particles to release fatty acids
  94. What is the rate-limiting step of beta-oxidation of fatty acids?
    Carnitine Shuttle
  95. Beta-oxidation of fatty acids takes place in the inner mitochondrial matrix where the enzymes that mediate this process are located. The inner mitochondrial membrane is not permeable to CoA or derivatives of CoA. How is this transport problem solved?
    Carnitine Shuttle: a co-transporter that transfers fatty acyl carnitine into the matrix in exchange for free carnitine
  96. Carnitine is obtained from the diet, or synthesized in the liver and transported to other tissues. _______ has the highest concentration of carnitine because it has the highest concentration of mitochondria and highest rate of beta-oxidation.
  97. This is a congenital syndrome resulting from abnormal synthesis of carnitine or impaired cellular uptake of carnitine. The deficiency can be systemic or in muscle only. This deficiency occurs most often in people who consume a complete _____ diet. If this is systemic, it prevents synthesis of _______.
    • Carnitine Deficiency Syndrome
    • Vegan
    • Ketones
  98. What molecule inhibits the Carnitine Shuttle? This prevents oxidation of fatty acids to take place under conditions when fatty acid synthesis is occuring
    Malonyl CoA
  99. The beta-oxidation pathway is a multi-step pathway that sequentially reduces a 16-C fatty acid by ___ carbons at a time.
  100. A carnitine-palmitoyl transferase-___ deficiency affects fatty acid oxidation in liver. This impairs gluconeogenesis during fasting.
    Carnitine-palmitoyl transferase-I
  101. A carnitine-palmitoyl transferase-___ deficiency occurs primarily in muscle and heart. This is accompanied by muscle weakness and intolerance to fasting.
    Carnitine-palmitoyl transferase-II
  102. This is the most common inborn error of metabolism. Beta-oxidation proceeds until the fatty acyl chain has been shortened to medium acyl chain length. The partial oxidation products are excreted in urine as carnitine esters. People with this deficiency are reliant on a high carbohydrate diet, and unable to tolerate long periods of fasting.
    Medium-Chain Fatty Acyl CoA Dehydrogenase Deficiency (MCAD)
  103. What is an alternative form of fuel that can be used by several tissues in the body? These are produced only in the liver, and can be used by most tissues, but cannot be used by the liver.
    Ketone Bodies
  104. This is the formation of ketone bodies from acetyl CoA
  105. What three molecules make up Ketone Bodies?
    • Acetoacetate
    • 3-hydroxy butyrate (formed by reducing acetoacetate)
    • Acetone (a nonmetabolized side product that forms in blood from acetoacetate)
  106. Ketone body synthesis occurs during _________ when the rate of beta-oxidation of fatty acids exceeds the capacity of the tricarboxylic acid cycle to fully oxidize acetyl CoA. Flux through the tricarboxylic acid cycle is diminished because _________ is being used for gluconeogenesis.
    • Fasting
    • Oxaloacetate
  107. The purpose of ketogenesis is to regenerate a pool of free ______ _____.
    Acetyl CoA
  108. This is the synthesis of compounds from Krebs cycle intermediates
  109. When gluconeogenesis is high, the ________ pathways are reducing the number of Krebs cycle intermediates and reducing the ability of acetyl CoA to be oxidized through the Krebs cycle
  110. In the fasted state, _________ is the major cataplerotic pathway.

    In the fed state, _________ is the major cataplerotic pathway.
    • Gluconeogenesis
    • De novo fatty acid synthesis
  111. In the fasted state, amino acids feed into the Krebs cycle to produce ________, which can then be used for gluconeogenesis.
  112. Where does synthesis of ketone bodies occur within the liver cell?
    Mitochondrial Matrix
  113. Why can't the liver use ketone bodies?
    Because it does not have thiophorase
  114. The adaptations that occur during the fasted state are driven by _____ levels of insulin, ______ glucagon, _____ epinephrine, and ______ cortisol levels as fasting proceeds.
    • Low
    • High
    • High
    • High
  115. When switching from glycolysis to beta-oxidation when converted to the fasting state, what cycle is responsible for shutting off fatty-acid synthesis? This causes glycolysis to be shut off by shutting off the flow of carbs into muscle.
    Randle Cycle
  116. The human body is only about ____% efficient in converting food into work.
  117. What are the three main energy sources of working muscles?
    • Phosphagen System
    • Anaerobic Glycolysis
    • Oxidative Metabolism of Lipids and Carbohydrates
  118. In the phosphagen system (energy-rich phosphate compounds), ATP is the substrate for myosin. All ATP can be hydrolyzed in ___ to ___ seconds. The ATP pool can be regenerated from the _______ _______ pool in muscle. This can supply ATP for _____ to ______ seconds.
    • 2-4 seconds
    • Creatine Phosphate
    • 6-20 seconds
  119. The second energy source for working muscles is anaerobic glycolysis from blood glucose and stored muscle glycogen. This supports vigorous activity from ___ seconds to ___ minutes. This pathway does not require oxygen, so ______ _____ will build up. Acidification of tissues will result in pain following the bout of activity.
    • 20 seconds to 2 minutes
    • Lactic Acid
  120. Anaerobic exercise is typified by sprinting or weight lifting. This activity is dominated by the activity of the ______-_______ muscle fibers. These fibers are ________.
    • Fast-twitch (Type II)
    • Glycolytic
  121. The third energy source for working muscles is oxidative metabolism, which is approximately 10x more efficient than the anaerobic glycolysis. However, it is limited by what?
    The major fuels for this type of exercise are ______ _____ and ______, which are metabolized to completion (no lactate build-up). This can only occur during aerobic exercise.
    • Limited by the oxygen supply to the tissues
    • Fatty Acids
    • Glucose
  122. Aerobic exercise is typified by long-distance running, swimming, etc. It involves prolonged activity that is carried out at a lower intensity, but long duration. This type of exercise involves what type of muscle fibers? They have an abundance of mitochondria, and appear red due to what?
    • Type I, Oxidative Muscle Fibers
    • High Myoglobin Concentration
  123. Metabolism in exercise is under what type of control? The sympathetic nervous system regulates blood flow to increase perfusion of the working muscles
  124. __________ is regulated by muscle contraction and catecholamines
  125. _______ release precedes the exercise activity and prepares the muscle for activity by starting to activate the glycogenolysis cascade.
  126. The nerve impulse resulting from muscle contraction signals the release of ________ from the sarcoplasmic reticulum, which activates ________ _________.
    • Calcium Ions
    • Phosphorylase Kinase
  127. Fatty acid oxidation is important in endurance exercise. The fatty acids are derived from ______ ______. Lipolysis of triacylglycerol stores adrenergic stimulation by the sympathetic nervous system.
    Adipose Tissue
  128. Fatty acid oxidation provides about ___% of the total energy required for high intensity endurance exercise. The remaining energy comes from where?
    • 60%
    • Muscle Glycogen Utilization
  129. Why doesn't the liver provide significant glucose for exercise?
    Because blood is diverted away from the liver by the sympathetic nervous system, thus reducing the contribution of hepatic glucose output during the exercise activity
  130. Is the Cori cycle active during exercise?
    No. Lactate that is produced in muscle cannot be converted to glucose via the Cori cycle during exercise. The Cori cycle wil be active after exercise
  131. Intensity: work done/ unit of time. This is also referred to as power.

    Light exercise is ____ W
    Moderate exercise is _____ W
    Heavy exercise is ______ W
    • 65 W
    • 130 W
    • 200 W
  132. Intensity of exercise can be judged by measurement of the rate of oxygen consumption (VO2 max). Intense exercise is carried out at about _____% VO2 max. Light exercise would be about ____% VO2 max.
    • 65%
    • 25%
  133. ______ ______ is required for maintaining aerobic power during intense exercise. Light exercise will not mobilize these stores.
    Muscle Glycogen
  134. Substrate utilization of muscle can be measured by indirect calorimetry. This measuers CO2 production/ O2 consumed, also known as the Respiratory Quotient (RQ).

    An RQ of ____ means that only carbohydrate is being used.
    An RQ of _____ measn that only fat is being oxidized.
    • 1.0
    • 0.7
  135. This type of fat distribution is characterized by a waist to hip ratio of >0.8 for women, and >1.0 for men. This is associated with increased visceral obesity and metabolic diseases.
  136. This type of fat distribution is associated with lower body obesity largely due to increased subcutaneous fat. This is not as tightly linked with metabolic disease.
  137. ________ adipocytes are more metabolically active, and tend to mobilize fatty acids more rapidly than _________ adipose. The cytokines that are secreted from adipocytes enter the portal circulation more rapidly when they are secreted from _______ adipose.
    • Visceral
    • Subcutaneous
    • Visceral
  138. What three cytokines are secreted from adipose tissue?
    • Adiponectin: main one. Increases insulin sensitivity
    • Leptin: signals CNS about the size of the adipose mass (increases as fat masses increase)
    • Resistin: reduces glycemic control
  139. How does the size and number of adipocytes change as weight gain increases?
    Moderate gain is associated with increased size of adipocytes, which is easily reversible. Long term overnutrition is associated with growth and development of new adipocytes, increasing cell number, which is less easily reversed
  140. Body mass is based on energy balance (the difference between energy intake, and energy expenditure). We gain weight when we are in ________ energy balance (intake _____ than output) and we lose weight when in ________ energy balance (intake _____ than output)
    • Positive (greater)
    • Negative (less than)
  141. What are the two genetic contributions (or evidence for them)?
    • Body mass correlates more with size of biological parents than adoptive parents
    • Some rare single gene mutations can cause human obesity (esp within Leptin system)
  142. This is an adipocyte-derived peptide hormone that crosses the blood-brain barrier. The hypothalamus has cell-surface receptors that bind it, and signal a cascade of events that lead to reduced food intake and increase in energy expenditure. This helps regulate body mass.
  143. What is the effect of insulin during hyperinsulinemia?
    Acts on hypothalamic neurons to dampen food intake
  144. Short-term signals from the intestinal tract control hunger and satiety, and are useful for signaling cessation of a specific meal. These factors are secreted by the gut or stomach and ultimately signal through hypothalamic neurons. What are they?
    • Cholecystokinin (CCK): secreted by intestine during a meal; anorexigenic factor to signal satiety
    • Peptide YY (PYY): secreted by intestine during a meal; anorexigenic factor to signal satiety
    • Ghrelin: secreted by the stomach when it's empty; orexigenic factor that stimulates meal-eating
  145. This is a constellation of metabolic abnormalities that include:
    Glucose Intolerance
    Insulin Resistance

    What can it lead to?
    • Metabolic Syndrome
    • Can lead to Type II Diabetes
  146. What is the key to maintaining weight loss, and improving hypertension? This alone does not reduce body mass, however. This must be done in conjunction with a calorie-restricted diet. Together, this can prevent development of full-blown __________.
    • Exercise (creates an energy deficit by increasing ATP turnover in muscle)
    • Type II Diabetes
  147. To lose one pound, you need an energy deficit of _______ calories.
  148. A solid goal for weight loss is to achieve ____% loss over a ____ month period of time. This is more maintainable because it is a gradual loss
    • 10%
    • 6 month
  149. What are the three types of calorie-restricted diets utilized for weight loss?
    • Ketogenic Diet
    • Low Fat Diet
    • Low Carbohydrate, High Protein Diet
  150. How does a Ketogenic Diet work?
    Restricted carbohydrate consumption leads to increased beta-oxidation of fatty acids in liver, and increased reliance on ketones
  151. This is a chronic progressive disease resulting from chronic insulin resistance and relative deficiency of certain physiologic actions of insulin
    Type II Diabetes
  152. What are the three factors that contribute to insulin resistance and Type II Diabetes?
    • Insulin resistance in the liver: leads to increased glucose production
    • Decrease insulin-mediated glucose uptake in adipose tissue and muscle: there is also decreased inhibition of the hormone sensitive lipase in adipose tissue leading to increased release of free fatty acids from adipose tissue
    • Inadequate secretion of insulin from beta cells of the endocrine pancreas
  153. Insulin resistance develops with obesity. When does it progress to full-blown diabetes?
    If islet cells begin to fail, and don't secrete enough insulin to compensate for resistance to the actions of insulin
  154. To detect insulin resistant, what type of insulin levels should be measured?
    Plasma insulin levels in the fed state
  155. Insulin resistance in the liver primarily affects __________. Insulin is not able to suppress it, so there is a high rate of glucose secretion.
    On the other hand, insulin is able to activate de novo fatty acid synthesis and cholesterol synthesis, so there is a high level of _______ particle secretion that is loaded with cholesterol.
    • Gluconeogenesis
    • VLDL
  156. This is an autoimmune disease that results in destruction of the islet cells of the pancreas. These cells are the endocrine cells responsible for secreting insulin. The islet cells are made up of alpha, beta, and delta cells. It is the beta cells that produce and secrete insulin.
    Type I Diabetes
  157. When is the clinical disease associated with Type I Diabetes manifested?
    The slow destruction of the beta cells can occur over a long period of time. Clinical disease is manifested when secretion of insulin dips below a critical threshold
  158. What are the symptoms associated with Type I Diabetes?
    • Polyuria (excessive urination): results from loss of glucose and ketones in the urine
    • Polydipsia (excessive thirst): results from dehydration and high solute concentration in blood
    • Polyphagia (excessive hunger): results from signals to the CNS that the body is starving
    • Muscle Weakness: present because insulin is not stimulating synthesis of new proteins, but muscle proteins are being broken down
    • Adrenergic Hormones: can lead to changes in heart rate, sweating, anxiety, and nausea
  159. In Type I Diabetes, energy substrates are not properly metabolized and stored. There is no insulin-responsive ________ uptake into adipose tissue, heart, or skeletal muscle. In addition, when taken up into the liver, it is not converted into glycogen or new fatty acids.
  160. In Type I Diabetes, energy substrates are not properly metabolized and stored. Fats are being mobilized from adipose tissue and also coming from the diet, so fatty acids are being taken up by the liver and resynthesized into _____ particles that do not contain much _________. The fatty acids are being oxidized in the liver, and converted to ketones at an excessive rate.
    • VLDL
    • Cholesterol
  161. In Type I Diabetes, energy substrates are not properly metabolized and stored. Proteins that are broken down in muscle are sending ______ _______ back to the liver for gluconeogenesis
    Amino Acids
  162. In Type I Diabetes, energy substrates are not properly metabolized and stored. _________ are slow to turnover because their cargo cannot be delivered to adipose tissue. Adipose tissue secretes a lipoprotein lipase when insulin levels are high. Without the lipoprotein lipase, the triacylglycerol content of __________ cannot be cleaved and taken up by adipose tissue.
    • Chylomicrons
    • Chylomicrons