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BioMedChem Midterm 1 > 9 - Biochemistry of Diabetes > Flashcards

9 - Biochemistry of Diabetes Flashcards

1
Q

Alpha

Cell Types of the Pancreatic Islets of Langerhans

A

Glucagon

pro-glucagon

GLP 1/2

20% of cells

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2
Q

Beta

Cell Types of the Pancreatic Islets of Langerhans

A

Insulin

C- Peptide (biomarker)

proinsulin

Amylin

75 % of cells

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3
Q

Delta

Cell Types of the Pancreatic Islets of Langerhans

A

Somatostatin

3-5% of cells

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4
Q

G / F (PP)

Cell Types of the Pancreatic Islets of Langerhans

A

Gastrin

Pancreatic Peptide (F)

~1% of cells

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5
Q

Somatostatin

A

from Delta cells, UCN3

Inhibits secretion of BOTH

Insulin

Glucagon

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6
Q

Amylin

A

From Beta cells

Co-secreted W/ Insulin

  • Slows Gastric Emptying*
  • Inhibits gastric secretions*
  • Inhibits GLUCAGON secretion*

Smooths out abrupt rises in BG after meal

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7
Q

Gastrin

A

From G cells

Stimulates secretion of

Gastric Acid + Pepsin

Gastric motility

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8
Q

GLP-1

A

from Alpha cells

weak secretagogue for -> Insulin

~promotes its release

Glucose Uptake consequentally

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9
Q

GLUT

A
  • Specialized Transmembrane proteins
    • similar to enzymes (characterized by Km / Vmax)
    • but NO Chemical Action on glucose
      • ​= Passive (but some active)
  • ​Glucose uptake = Rate limiting Step
    • in glucose utilization & Storage
      • = GLUT are KEY transporters in metabolism
  • Some are found on _kidney_
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10
Q

GLUT1

A

Ubiquitous (everywhere)

1.5mM

basal glucose uptake

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11
Q

GLUT2

A

15-20mM = low affinity

Intestine

Liver = remove excess glucose

Pancreas = regulate insulin release

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12
Q

GLUT3

A

Brain

1mM = highest affinity / most sensitive

glucose uptake

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13
Q

GLUT4

A

Muscle / Fat / heart

5mM

Activity INCREASED by INSULIN

more glucose brought into by insulin binding

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14
Q

GLUT5

A

Intestine / Testis / KIDNEY / Sperm

Mainly Fructose transport

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15
Q

Causes of T2DM

A
  • Defects in 1+ pathways including:
    • Signaling / Metabolic pathways
  • ​​​~10 genes implicated
    • Genetic & Environmental
  • Correlated w/ exogenous stimuli (environmental factors)
    • IRON overload
    • Glucocorticoid treatment
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16
Q

How is OBESITY linked with DM?

A
  • Obesity -> Visceral Fat -> Insulin resistance in peripheral tissues
    • Upsets in lipid metabolism
      • Close connection of lipid & glucose metabolism
  • Sedentary life / High calorie diet
    • Strong correlation between DM & Obesity
17
Q

How do “Thrifty Genes” contribute to DM/Obesity

A
  • Early times, starvation was an issue:
    • When food was abundant:
      • calories were stored as FAT (TG’s)
        • Fat was Denser energy source than glycogen
18
Q

Randle Diet / Hypothesis

A

Possible cause for Insulin Resistance & Obesity

  • Increase in Carb (Sugar) & FA (Fats) metabolism
    • ​more Acetyl CoA + Citrate
    • Citrate inhibits PFK
    • Acetyl CoA inhibits Pyruvate Dehydrogenase (PDH)
      • ​-> reduction in the rate of Glycolysis
        • ​INTRACELLULAR GLUCOSE + G6P RISES
          • ​GLUT4 slows, hexokinase inhibited
            • less glucose uptake
19
Q

Randle Hypothesis: Fatty Acid Side

A
  • LCFA undergoes Beta Oxidation in Mito
    • -> Acetyl-CoA buildup
      • negative feedback, inhibits PDH
        • ​pyruvate -/-> acetyl-CoA
    • ​​Acetyl-CoA -> CITRATE -> Cyto
      • ​inhibits PFK-1 & GLUT4
        • ​**less glucose intake & G6K conversion
20
Q

Randle Hypothesis: Glucose Side

A
  • Glucose metabolism -> Pyruvate ->
    • Acetyl-CoA buildup in Mito->Cyto
      • -> buildup of MALONYL-CoA
        • ​inhibits CPT-1
          • less FA transport to MITO
            • ​buildup of Fatty Acids in cytosol
  • ​​​​​Cytosolic FA (DAG / Ceramide) stress ER:
    • Release Cytokines
    • FA stores as TGs in fat droplets -> OBESITY
21
Q

Malonyl CoA

A
  • Buildup of Malonyl-CoA (is from Acetyl-CoA)
    • ​which then blocks CPT-1
      • reduces FATTY ACID TRANSPORT into the MITO
        • buildup of Cytosolic FA’s
          • ​converted to -> DAG / Ceramide
22
Q

DAG & Ceramide

A
  • Malonyl CoA Buildup inhibits CPT-1
    • which results in a buildup of Cytosolic FA’s (convert to DAG / Ceramide)
      • Bind to Stress Induced Ser-Kinases
        • ​-> competitively inhibit INSULIN RECEPTORS
          • -> less GLUT4 to take in glucose
  • Insulin receptors are also Ser-Kinases
    • DAG & Ceramide binding to these interferes with the signal transduction pathway of insulin
23
Q

Insulin Resistance in Muscle

similar to randle hypothesis

A
  • Increase in DAG / Ceramides / Fatty Acyl coA
    • bind to SER / THR Kinases -> Cascade
      • instead of Tyr-kinases
      • ​​​​Insulin normally binds to Tyr Kinase Receptor
        • ​but there is less of it phosporylated due to the Ser/Thr Kinase cascade
          • -> Less GLUT4 Activity
            • ​Insulin Resistance
24
Q

How Insulin Resistance leads to T2DM

A
  • Insulin Resistance -> Beta cell compensation
    • ​-> more INSULIN secreted but no effect
      • increase in Gluconeogenesis (more GLUCOSE)
      • increase in Lipolysis in visceral fat
        • normally insulin would supress these
  • ​​​Beta Cells DEcompensated (stressed, not working)
    • -> decrease in INSULIN Synthesis / Secretion
      • ​​​Glucose buildup & impaired glucose tolerance
25
Q

Causes of Type 1 DM

A
  • Loss of Beta-Cells due to:
    • viral infection / environmental triggers
      • ​-> immune system attacks the cells
  • Chemical Triggers:
    • Zinc Chelators
    • Nitrates
    • Rodenticides
26
Q

Type 3 DM

A

Elevated Blood Glucose not caused by insulin resistance

  • Genetic Defects on:
    • beta cell fxn
    • insulin action
  • Diseases of the exocrine pancreas
  • Drugs / Chemicals (rat poison)
  • Endocrine Disorders
27
Q

Rare Causes of DM: Endocinopathies

A
  • Some Increase Insulin Resistance:
    • Acromegaly / POS
    • HYPERthyroidism
    • ​Cushing’s Syndrome
      • hypercortisolism
  • Some DECREASE Insulin Secretion:
    • ​somatostatinoma
    • aldosteronoma
    • pheochromocytoma
28
Q

Gestational DM

A
  • ~4x increase in INSULIN secretion demand for pregnancy
    • Mother does not secrete enough insulin
      • can not compensate for higher metabolic demands & glucose output
  • 4% of all pregnancies
    • H/O diabetes increase risk
    • Increase risk of stillbirth
29
Q

Diabetes Insipidus

A
  • Urine W/o taste; no glucose
  • Defect in Aquaporin-2 (AQP-2)
    • becomes insensitive to vasopressin
      • ​-> little water is reclaimed in kidney
        • ​MORE “dilute = insipid” URINE is passed
30
Q

Aquaporin-2

AQP-2

A
  • Epithelial Protein in Kidney
  • Vasopressin stimulates its action of:
    • Increases in water re-absorption in kidney
      • when vasopressin falls -> there is more water in the urine excreted
  • ​​DEFECT in AQP-2
    • ​-> Diabetes Insipidus
31
Q

How does T2DM affect Hypertension

A
  • T2DM -> High Blood Glucose Concentration
    • ​increase in Osmotic Pressure
      • -> Increase BP
  • Polyuria from filtering out glucose
    • -> leads to Polydipsia
    • -> increased rate of filtration of PROTEINS
      • -> damage to kidney
        • pore size increase
        • glycosylation
32
Q

Polyuria

A

Large Amounts of URINE

–> Polydipsia (thirst)

  • Can be caused by T2DM
    • due to kidney’s need to filter out GLUCOSE
  • Polyuria effects:
    • -> Increased rate of filtration of Proteins
      • ​Increase in Pore Size / Urinary Space
    • ​-> Kidney Damage
      • Glycosylation of enzymes/transporters
        • caused by HIGH BG
33
Q

How does T2DM cause Glycosylation & Tissue Damage?

A
  • High Blood Glucose
    • ​-> Glycosylation of proteins
      • -> produce AGE’s
  • ​​AGE’s damage cell by altering enzymatic/binding activity of cellular proteins
    • -> abnormal interactions in matrix
      • -> Tissue Adhesion
      • -> Recognition Systems
        • ​of Blood Vessels / Nerves / Organs
34
Q

AGE’s

A

Advanced Glycosylation End Products

  • Can be made due to HIGH Blood GLUCOSE
    • -> increase in glycosylation of proteins
      • -> AGE’s
  • Affect Tissue Adhesion & Recognition Systems
    • of BV’s / Nerves / internal organs
      • ​by altering enzymatic / binding activity of proteins
35
Q

Trauma’s effect on Diabetes

A
  • Trauma -> release of stress hormones:
    • Catecholamines + Cortisol
      • ​raise level of CATABOLISM
  • -> Supress Insulin Release
    • -> more Glucose
    • -> more lipolysis -> more FFA
      • –> HYPERGLYCEMIA & KETOSIS
        • _​_esp important consideration for DM patients
36
Q

Why do DM patients require special consideration for surgery?

A
  • TRAUMA -> stress hormones + Supression of Insulin release
    • Catacholamines + Cortisol
      • -> increase in Catabolism
    • –> HYPERGLYCEMIA
    • ​​KETOSIS
37
Q
A

BioMedChem Midterm 1 (9 decks)

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