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BioMedChem Midterm 1 > 5 - Obesity & Metabolic Syndrome > Flashcards

5 - Obesity & Metabolic Syndrome Flashcards

1
Q

BMI

A

Body Weight (kg)

————-

Height (m2)

Classifies OBESITY

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2
Q

Metabolic Abnormalities that make up Obesity

A
  • Insulin Resistance
  • Beta-Cell Failure
  • Dyslipidemia
    • ​High TG’s / low HDL / dense LDL
  • Non-alcoholic Fatty-Liver Disease
  • NOT SYNONYMOUS
    • ​You can be obese even though you have normal metabolism
    • Obesity is simply BMI>30 (kg/m2)
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3
Q

Obesity & Genetics

A

Obesity is MULTIFACTORAL

  • Some evidence of genetic contribution
    • Numerous genese assoiated w/ :
      • weight gain / BMI changes
  • Epigenetic risk factors also important
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4
Q

Enlarged Adipocytes produce:

A
  • Obese patient’s large adipocytes
    • produce larger amounts of ​Adipokines
    • promote inflammation
    • increase insulin resistance​
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5
Q

What factors impact weight?

A

Insulin Resistance

Inflammation

GUT MICROBIOME

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6
Q

Leptin & Obesity

A
  • Leptin is the key regulator of the brain-gut axis
  • Activation of the hypothalmic leptin receptors:
    • ​Blocks food intake
    • Increases expenditures
  • ​Leptin decreases with weight reduction
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7
Q

Genes that encode for what underlie Obesity?

A
  • Leptin
  • Leptin Receptor (LEPR-B)
  • Insulin
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8
Q

Obesity Physiology Pathway

A
  • Imbalance in Caloric Intake & Energy expenditure
    • ​-> Positive energy Balance
      • -> Inflammed Adipose Tissue
        • ​-> Increased FFA release to:
          • ​Liver
          • Pancreas
          • Muscle
          • Epicardium__​​​
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9
Q

Obesity effects on the LIVER

A
  • Accumalation of intrahepatic TG’s
    • -> reduced sensitivity to Insulin
      • ​​​in muscle / liver / adipose tissue
  • _​​_Excess FFA​ from adipose tissue
    • -> hepatic & skeletal Insulin resistance​
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10
Q

Metabolic consequences of more circulating FFA from adipocytes

A
  1. Less Glucose uptake in muscles
  2. More Glucose uptake by Liver
  3. Change in Gut microbiome
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11
Q

How does obesity drive Insulin Resistance?

A
  • Liver
    • _​_Making too much Glucose
      • ​gluconeogenesis + lipotoxcity
  • ​Skeletal Muscle
    • ​Reduced Glucose Uptake
      • ​due to it taking in more Lipids
      • insulin action is reduced
  • Chronic Hyperinsulinemia
    • Desensitizes Insulin receptors
  • ​Low level inflammation -> cytokine release
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12
Q

How does inflammation lead to insulin resistance?

A
  • Chronic low-grade inflammation in obesity
    • -> increase in Cytokines ( TNF-alpha )
      • ​activates JNK + NF-KB
        • -> dephosphorylation of Insulin Receptors
          • also IRS inhibition by JNK
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13
Q

VMN

Ventro-medial hypothalamic nucleus

Signaling in the Hypothalamus

A
  • VMN Stimulation
    • -> Supression of food intake
  • ​Lesions in VMN -> induce Obesity
  • Regulated by Leptin & Insulin
      • NPY
    • + Ghrelin
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14
Q

Obese Individuals produce more ____ than normal people

A
  • Leptin
    • ​block food uptake
  • TNF-alpha
  • IL-6
  • PAI1
  • less Adiponectin
    • ​healthy individuals produce more adiponectin
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15
Q

ARH

Arcuate Hypothalmus Nucleus

Signaling in the Hypothalamus

A
  • Stimulation of ARH
    • ​-> INCREASED food intake
  • Damage of ARH -> reverses it
  • NPY / AgRP Neurons
    • ​+ Ghrelin
      • ​stimulates appetite
    • - Leptin
      • ​inhibits it
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16
Q

NPY

Neuropeptide Y

Signaling in the Hypothalamus

A
  • Stimulates hypothalmic regulation of food intake
  • Increases Obesity
  • Decreases total energy expenditure
  • NPY gene expression is inhibited by Leptin
17
Q

Leptin

Signaling in the Hypothalamus

ARH

A
  • Inhibits ARH NPY Gene Expression
    • ​**–> Reduction in **Obesity
    • reduced Hunger / weight
  • ​Leptin Resistance
18
Q

Ghrelin

Signaling in the Hypothalamus

ARH

A
  • Peptide hormone produced by the STOMACH
    • ​Physically senses when stomach is empty
  • ​​STIMULATES APPETITE
    • ​–> causes weight gain
  • Regulates NPY & AgRP in hypothalmus
19
Q

How does Obesity affect Metabolism?

A
  • Impairment of Glucose Transport into muscle / adipose tissue
    • _​_downregulation of GLUT4
  • ​​​Increase in Basal Lipolysis
    • ​–> increase in FFA
  • ​protein metabolism is still controversial
20
Q

Obesity on inflammation

A
  • Obese Adipose -> Increase in Macrophages
    • ​-> Increase in pro-inflammatory cytokines
  • ​TNF-Alpha
    • ​contribute to insulin resistance
      • ​Anti-TNF therapy in animals increase insulin sensitivity
    • Reduce GLUT4 expression
21
Q

Why is there more LEPTIN in Obese tissue?

A

LEPTIN RESISTANCE

there is also less ADIPONECTIN in obese tissue

22
Q

Possible treatments to ​REDUCE OBESITY

A
  • Leptin​
    • ​also inhibits NPY
    • but there is leptin resistance
  • ​GLP-1 Receptor Agonist
    • -> stimulate insulin release
  • Anti-TNF
  • Anti-Ghrelin
23
Q

Pharmacotherapies for Obesity

A
  • Appetite-Supressants
    • ​Phentermine / topiramate
  • Lorcaserin
  • Naltrexone / Bupropion
  • Liraglutide = GLP-1 Receptor Agonist
  • ​Serotonergic drugs / Cannabinoid receptor antagonist
    • ​no longer approved
24
Q

Metabolic Syndrome’s associated risk factors:

A
  • impaired Fasting Glucose
  • Abdominal Obesity
  • Hypertension
  • Dyslipidemia
25
Q

Viceral Fat

A

Increases chance for Metabolic Disease

  • Fat that surrounds your organs
  • linked to :
    • heart disease
    • T2DM
    • Strokes
26
Q

Hip to Waist vs BMI

H2W

A
  • Waist / Hips = H2W Ratio
    • ​More Indicative since it shows WHERE the fat is stored
    • more viceral fat is in the stomach
  • BMI is just weight / height
27
Q

Insulin Action in MS (metabolic syndrome)

A
  • Pancreas
    • ​Insulin Resistance
      • ​-> contribute to MS
    • Accumalation of FA’s
      • ​-> Diminished insulin production
  • Viceral Obesity -> Insulin resistance
    • -> Blood Clots & CVD​
28
Q

Leptin Functions

A
  • Control peripheral energy status
    • Reduce Appetite
    • Improve Insulin Sensitivity
    • Increase ENergy Expenditures
29
Q

3 Main Causes of Insulin Resitance

A
  • Leptinemia
    • increased synthesis
  • Reduction of leptin’s access to the CNS
    • ​due to BBB
  • Disruption of signaling
    • Impaired ObRB downstream signal transduction
    • reduction in OrRB expression @ plasma
    • reduction in Positive regulators
    • INCREASE in NEGATIVE receptors
30
Q

ObRB

A

Leptin Receptor in the Brain

31
Q

Adiponectin & MS

A
  • levels are reduced in Obesity
  • Adiponectin functions:
    • May increase insulin sensitivity
    • Suppresses Glucose in the liver
    • Enhances FA Oxidation in the muscle__​​​
32
Q

Lipid Metabolism & MS

A
  • Dyslipidemia is associated w/ MS
    • high TG’s + FFA’s
    • decreased HDL
33
Q

HDL in MS

A
  • ​HDL particles are smaller in visceral obesity & MS
    • due to lipoprotein binding more TG vs cholesterol
    • Enhances HDL delivery of lipid to LIVER
      • _​_forms small dense particles that Stimulate macrophages & trigger inflammation
        • Promotes ARTERIOSCLEROSIS
34
Q

What increases risk for CVD & Artherosclerosis?

A
  • Metabolic Syndrome
    • ​Dyslipidemia / HT / Insulin Resistance
  • Diabetes
  • Non-Alcoholic Faty Liver Disease (NAFLD)

BioMedChem Midterm 1 (9 decks)

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