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Biochem Spring > Chapter 20- Perturbations of Energy Metabolism: Obesity and Diabetes Mellitus > Flashcards

Chapter 20- Perturbations of Energy Metabolism: Obesity and Diabetes Mellitus Flashcards

1
Q

What is intermediary metabolism?

A

all changes that occur in a food substance beginning with absorption and ending with excretion

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2
Q

What are the energy content of carbohydrates, protein, fat, and alcohol?

A

Carbohydrate 4, protein 4, fat 9, alcohol 7kcal/g

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3
Q

BMR is increased in what diseases?

A

hyperthyroidism, fever, Cushing’s syndrome, tumors of adrenal gland, anemia, leukemia, polycythmia, cardiac insufficiency, & injury

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4
Q

BMR is decreased in what diseases?

A

hypothyroidism, starvation, malnutrition, hypopituitarism, hypoadrenalism (Addison’s disease), and anorexia nervosa

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5
Q

Integration of signals for energy storage and dissipation are mediated by what?

A

Hypothalamus

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6
Q

what is AMPK?

A

heterotrimeric protein complex and consists of a catalytic alpha-subunit and regulatory beta and gamma subunits

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7
Q

When AMP levels rise during anabolism what happens to AMPK?

A

AMPK is allosterically activated -> promotes ATP synthesis by activating key regulatory enzymes in the catabolic pathways

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8
Q

Negative allosteric regulators of AMPK are?

A

phosphocreatine and glycogen

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9
Q

MOA of metformin

A

activates AMPK -> inhibits the transcription of key regulatory hepatic enzymes required for gluconeogenesis

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10
Q

What is leptin?

A

Long-term regulator of energy store in adipocytes, functions in the afferent signal pathway of - feedback loop in regulating the size of adipose tissues & energy balance

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11
Q

Where is leptin synthesized?

A

adipocytes

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12
Q

how is leptin synthesis increased?

A

insulin, glucocorticoids, & estrogens

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13
Q

What happens when leptin levels are low

A

starvation, [low leptin] -> production of neuropeptide Y from hypothalamus, transported to paraventricular nucleus (PVN) of hypothalamus -> ↑appetite, & ↓ energy expenditure, Temp, reproductive function, and ↑ parasympathetic activity

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14
Q

What happens when leptin levels are high?

A

[↑leptin] -> opposite set of reactions ↓NPY -> activates POMC pathway-> mediated by MSH binding to MC4-R -> initiate reactions, ↓appetite, ↑energy expenditure, and sympathetic activity

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15
Q

Leptin levels in obese individuals are?

A

High leptin levels in obese individuals -> due to resistance or defect in leptin receptors

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16
Q

What transcription factor regulates conversion of preadipocytes to adipocytes?

A

peroxisome proliferator-activated receptor-γ (PPAR-γ2)

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17
Q

what are thiazolidinadiones?

A

hypoglycemic agent given to diabetics, synthetic ligands for PPAR-γ2-> activates PPAR-γ2 -> adipogenesis, increase insulin sensitivity

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18
Q

BMI overweight and obese

A

BMI- 25-29.9 = overweight

>30= obese

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19
Q

Short term regulators of hunger and satiety are

A

plasma levels of glu & a.a., cholecystokinin & other hormones

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20
Q

only known appetite stimulating peptide hormone secreted by the stomach

A

Ghrelin, also stimulates GH secretion

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21
Q

early onset obesity can be characterized by

A

Congenital human leptin deficiency, defective leptin receptor gene-> high plasma leptin d/t defective leptin metabolism or leptin resistance

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22
Q

Prader-Willi syndrome:

A

the most prevalent form of dysmorphic genetic obesity, PWS is caused by absence of the paternally derived PWS/AS region of chromosome 15

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23
Q

Angelman syndrome:

A

inherited chromosome 15 deletions from mother

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24
Q

Obesity treatments

A

behavioral modifications, dietary restrictions, exercise, pharmacotherapy (sibutramine, orlistat), & surgical intervention (bariatric surgery)

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25
Q

what is orlistat?

A

pancreatic lipase inhibitor that prevents absorption of lipids from the GI tract

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26
Q

what is sibutramine?

A

serotonin reuptake inhibitor -> appetite suppressant

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27
Q

primary source of energy during exercise generating maximum power

A

ATP & P-creatine -> glycolysis from glycogen

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28
Q

Source of energy during High-intensity endurance exercise

A

P-creatine -> glycogenolysis (muscle & liver)->  increasing aerobic oxidation, FA & plasma glu utilization, BCAA oxidation

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29
Q

Source of energy during Low-level non-fatiguing exercise

A

similar to long endurance exercise but w/o depletion of P-creatine & minimal muscle glycogen utilization; aerobic oxidation of FAs, glu, & BCAA -> main source of Energy

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30
Q

metabolic homeostasis is regulated by

A

endocrine system

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31
Q

Metabolic role of liver

A
  1. 1st organ to meet nutrients delivered from the intestines (except Lipid), the secreted insulin & glucagon
  2. Deliver bile into the intestine: cholesterol Homeostasis
  3. The primary site of glycogen deposition & blood glucose maintenance
  4. Plays central role in lipid, protein, & Nitrogen homeostasis
  5. In the typical adult, the liver exports daily 180g of glucose, 100g of TG, & 14g albumin
  6. Metabolic energy supplied by fatty acid oxidation
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32
Q

Metabolic role of adipose tissue

A
  1. 13kg, increase -> obesity
  2. Brown Adipocyte: production of heat
  3. White Adipocyte: TG for export as FAs
  4. Synthesize TG from FA &; Glu
  5. Energy supplied by FA oxidation & TCA cycle
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33
Q

Metabolic role of skeletal muscle

A
  1. 35Kg, contain the major portion of the body’s nonlipid fuels
  2. Contains 4X as much glycogen as the liver
  3. Lacks G6Pase -> Can’t be a source of Blood Glu,
  4. During starvation, muscle provides a.a. -> the primary C source for glucose homeostasis
  5. Cori cycle; anaerobic metabolism Glycogen -> Lac -> Glu in the liver
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34
Q

Metabolic role of brain

A
  1. Constant metabolic fuel user
  2. ~20% total O2 consumed, 2/3 O2 to maintain transmembrane potential
  3. Glu, below ~50mg/dL -> dizziness & lightheadedness
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35
Q

Metabolic role of heart

A
  1. Aerobic, uses FAs (glu), Ketone bodies, lactate, & pyruvate -> “scavenger”
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36
Q

Metabolic role of kidneys

A
  1. Uses Glu, FAs, ketone, a.a.
  2. Important in a.a. homeostasis
  3. Has the same gluconeogenic capacity /g tissue as liver -> ~80% used for urine formation
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37
Q

Metabolic role of GI

A
  1. CHOs, TG, Protein -> use & store
38
Q

Metabolic role of blood

A
  1. Metabolites utilization and release coordinated
  2. Simple Monosaccharides, a.a. (high in Ala & Gln), Anions (lactate, pyruvate, acetoacetate, β-hydroxybutyrate), TCA intermediates, toxic metabolites (urea, bilirubin, creatinine, creatine), macromolecules (albumin, lipoproteins)
39
Q

Metabolic role of other body fluids

A
  1. Albumin: most abundant plasma protein, osmotic regulation, transport of FAs, drugs, & toxic metabolites, indicator of hepatic function
  2. Lipoproteins: complex of TG, protein, Cholesterol, & PLs
40
Q

Metabolic role of endocrine pancreas

A

Pivotal in metabolic homeostasis & integral component of metabolic regulation
α- & β-cells make up 20% & 75% of the total weight
Insulin, Glucagon, Somatostatin, Pancreatic polypeptide

41
Q

Structure of insulin

A

A & B chain + C peptide,

42
Q

Insulin synthesis

A

preproinsulin -> proinsulin -> secretary granules -> cleaves into Insulin + C-peptide by Enzyme

43
Q

C-peptide is a good measurement of

A

distinguishing endogenous versus exogenous insulin (determine how much insulin secreted by patient)

44
Q

Insulin secretion stimulants

A

Glucose, a.a., glucagon-like peptide (GLP), Ach, incretins, β-adrenergic agents stimulate, sulfonourea

45
Q

insulin secretion inhibitors

A

Somatostatin, α-adrenergic agents, diazoxides

46
Q

Familial hyperproinsulinemia

A

Genetic mutation where c-peptide remains attached to A chain (autosomal dominant trait); usually no symptoms of insulin resistance or hyperglycemia (maybe mild)

47
Q

What is Lispro?

A

Lispro insulin (no dimer formation, insulin of choice to treat diabetes)-> 28Pro29Lys on B chain are switched-> same biological activity-> reduced hexameter formation-> biological activity within 15 min of admin

48
Q

Biological actions of Insulin

A

Promote fuel storage & protein synthesis (inhibit breakdown)
Glucose uptake into muscle & adipose tissue via GLUT4 translocation

49
Q

Describe properties of Insulin Receptor

A

Heterotetramer, tyrosine kinase, P/deP gene regulation

50
Q

Describe Leprechaunism

A

receptor gene problem, type A insulin resistance

51
Q

short acting insulins are

A

Lisper, aspart, glulisine

52
Q

long acting insulin are

A

glargine, detemir

53
Q

Glucagon stimulates, inhibits, enhances what

A

Stimulates glycogenolysis, gluconeogenesis & ketogenesis in the liver, inhibit glycogenesis

Enhance lipolysis of TG in adipocytes to provide FFAs

54
Q

Glucagon secretion MOA

A

pancreatic alpha-cell membrane Receptor -> Gs protein complex -> AC activation -> increased cAMP -> cAMP dependent kinase (PKA) -> increased Phosphorylation of the controlling enzymes

55
Q

High ratio of insulin/glucagon induces

A

glucokinase, citrate cleavage enzyme, acetyl-CoA carboxylase, HMG-CoA reductase, pyruvate kinase, 6PF1K, 6PF2K, & F2,6BPase

56
Q

Low ratio of insulin/glucagon represses

A

glucokinase, citrate cleavage enzyme, acetyl-CoA carboxylase, HMG-CoA reductase, pyruvate kinase, 6PF1K, 6PF2K, & F2,6BPase

57
Q

Low ratio of insulin/glucagon induces

A

G6Pase, PEP carboxylase, F1,6BPase

58
Q

High ratio of insulin/glucagon represses

A

G6Pase, PEP carboxylase, F1,6BPase

59
Q

Secretion of glucagon triggered by

A

hypoglycemia, low blood [glucose], elevated [blood a.a.], exercise, inhibited by high blood [glu]

60
Q

Somatostatin synthesized by

A

synthesized in the δ cells of islets, gut, hypothalamus, & several other areas of the brain

61
Q

In the islets somatostatin does what?

A

blocks insulin & glucagon secretion

62
Q

Forms of somatostatin

A

2 forms, S14, S28 exist

63
Q

In the pituitary gland somatostatin does what?

A

inhibit GH & TSH release

64
Q

In the gut somatostatin does what?

A

blocks gastrin, motilin secretion -> inhibit gastric acid & pepsin secretion, suppresses gallbladder contraction -> lead to decreased delivery of nutrients to the circulation

65
Q

Pancreatic polypeptide is secreted when?

A

in response to fuel ingestion and potentially affect pancreatic exocrine secretion of bicarbonate and protein

66
Q

In islet cell regulation alpha-cell does what?

A

stimulates beta and delta cells

67
Q

In islet cell regulation beta cell does what?

A

inhibits alpha cells

68
Q

In islet cell regulation delta cell does what?

A

inhibits alpha and beta cells

69
Q

RBC’s only use what kind of glycolysis?

A

anaerobic glycolysis -> lactate

70
Q

At rest skeletal muscle use what for energy?

A

fatty acids

71
Q

In heavy exercise skeletal muscle use what for energy?

A

glycogen & blood glucose glucose must be available for these tissues

72
Q

Fructose is metabolized where?

A

part of fructose metabolized in intestinal cells, the rest enters portal blood, liver & kidney are the other sites of fructose utilization

73
Q

Fructose is absorbed on apical membrane on intestinal cells via?

A

GLUT5

74
Q

Fructose is absorbed on basolateral membrane intestinal cells via?

A

GLUT5 and GLUT2

75
Q

If diet consist of only CHO’s then glucagon levels

A

decrease

76
Q

If diet consist of high protein then glucagon levels

A

increase

77
Q

The liver converts excess glucose to

A

TG -> VLDL

78
Q

insulin directly stimulates glucose uptake by most cells except

A

brain, liver, and blood cells

79
Q

effects of insulin on glycogen synthase

A

activates glycogen synthase -> increased glycogen synthesis

80
Q

glucocorticoids do what

A

stimulate FA oxidation, gluconeogenesis, glycogenesis, ↑enzymes of glucagon action

81
Q

rapid stimulators of lipolysis

A

Epinephrine, glucagon within minutes

82
Q

slow stimulators of lipolysis

A

Growth Hormone, glucocorticoids’ action requires hrs

83
Q

inhibitors of lipolysis

A

Insulin & prostaglandin E1 suppress lipolysis by depressing cAMP levels

84
Q

under normal conditions the brain cannot use ketones because?

A

the enzyme needed is induced after 4 days of starvation

85
Q

in prolonged starvation what happens to gluconeogenesis?

A

liver gluconeogenesis↓, kidney gluconeogenesis↑ as the need for NH3 secretion↑

86
Q

Acarbose MOA

A

α-glucosidase inhibitor: inhibit breakdown of CHOs into glu by intestinal brush-border α-glucosidase & pancreatic lipase

87
Q

Metformin MOA

A

a biguanidine: inhibition of hepatic gluconeogenesis & glycogenolysis; in muscle, ↑insulin R tyr kinase activity & ↑GLUT4 transporter system -> adverse effect, lactic acidosis

88
Q

Troglitazone (TZD) MOA

A

↑insulin sensitivity in liver, muscle, & adipose tissue; promote conversion of non-lipid-storing preadipocytes to mature adipocytes with ↑insulin sensitivity; functions as TF targets PPAR-γ -> regulate expression of proteins controlling metabolic pathways, side effects -> hepatic toxicity

89
Q

SUR analog (repaglinide) MOA

A

inhibits different K+ channel -> rapid-onset & short-acting effects

90
Q

How is leptin synthesis decreased?

A

decreased by β-adrenergic agonists

Biochem Spring (8 decks)

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