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Biochem 4 > diabetes > Flashcards

diabetes Flashcards

exam 4

1
Q

little to no insulin production

A

diabetes

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2
Q

hallmark of diabetes

A

hyperglycemia

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3
Q

treat type II diabetes and it is an alpha-glucosidase inhibitor

A

acarbose

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4
Q

acarbose works by

A

slowing down the enzyme that converts carbohydrates to sugar; thus results in smaller blood glucose rise

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5
Q

SGLT2 Inhibitor

A

Jardiance

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6
Q

Jardiance works by

A

stoping glucose absorption from nephron back to blood

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7
Q

Initial protein structure of insulin, _______ is made in ER lumen

A

pre-proinsulin

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8
Q

is excised and proinsulin is transported to Golgi

A

Signal peptide

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9
Q

C-peptide can be used to

A

assess whether β cells are producing insulin; if it is present in blood then that means insulin is also being secreted

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10
Q

In Golgi, proinsulin is converted to insulin by removal of ___________ and enters secretory granules

A

C-peptide

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11
Q

Glucokinase is present in the

A

liver and pancreas

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12
Q

ATP will bind and activate a _____ that results in depolarization → Ca2+ release → Insulin vesicle release

A

K+ Channel

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13
Q

Sulfonylureas and Meglitinides can control diabetes by

A

interacting at the ATP K+ Channel

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14
Q

__________are peptide hormones that work to INCREASE INSULIN SECRETION (augment its effect) → REDUCES GLUCOSE

A

Incretins

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15
Q

Incretins are made by endocrine cells of the small intestine

A

L-Cells create GLP-1

K-Cells create GIP

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16
Q

incretins act on ____ and why?

A

pancrease to drive insulin secretio

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17
Q

GLP-1 will bind to GLP-1R (GPCR) and activate

A

adenylate cyclase

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18
Q

cAMP activates PKA which acts on

A

K+ channel, allowing membrane depolarization, Ca2+ influx and insulin secretion

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19
Q

is a stable GLP-1/GIP analogue that will help augment insulin secretion and treat Type II Diabetes

A

Exenatide

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20
Q

is a Dipeptidyl Protease IV inhibitor, it binds and stops the enzyme that breaks down GLP-1/GIP

A

Sitagliptin (Januvia)

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21
Q

leads to ketoacidosis

A

Type I

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22
Q

HONC- hyperoamolar non-ketotic coma/HHS- hyperglycemic hyperosmolar syndrome

A

Type II

23
Q
  • Autoimmune reaction of -ABs to pancreatic β-cells
  • Normal response to insulin, BUT NO insulin production
  • Severe hyperglycemia
  • Genetic susceptibility
A

Type I

24
Q
  • Commonly seen with obesity
  • Preserved β-cells
  • Little to high insulin production; but usually REDUCED insulin response
  • Genetic susceptibility
A

Type II

25
Q

can occur in some pregnancies; can cause effects in mother and child

A

Gestational Pregnancy

26
Q

Insulin reduces blood glucose in 3 ways:

A
  1. Causes translocation of GLUT4 receptors on muscle, fat, and white blood cells
  2. Suppresses glycogenolysis
  3. Suppresses gluconeogenesis
27
Q

is a drug that interacts with COMPLEX I of ETC and cause the increased formation of AMP

A

metformin

28
Q

AMP will bind to glucagon-receptor and

A

INHIBIT IT to prevent GLUCONEOGENIC PATHWAYS

29
Q

Glucose reacts with metals to generate

A

reactive oxygen species

30
Q

. The polyol pathway generates Sorbitol; the pathway will lead to an accumulate of Sorbitol which causes an

A

OSMOTIC EFFECT

31
Q

Glycation generates protein adducts (HbA1c) leading to advanced ___________ (AGE) that are themselves reactive.

A

glycation endproducts

32
Q

Can measure average blood glucose level with

A

HbA1c level

33
Q

Polyol pathway consumes

A

NADPH

34
Q

Insulin signaling involves

A

PROTEIN KINASE and LIPID SIGNALING

35
Q

Insulin will bind to its receptor, which is a ____________; when insulin receptor is active it will phosphorylate ITSELF and ADAPTOR PROTEINS

A

tyrosine kinase

36
Q

Ras will affect transcription factor kinases that will then cause changes in

A

transcription factors to drive gene transcription

37
Q

p-IRS-1 will activate __________in protein kinase

A

Ras (GDP → GTP active)

38
Q

Insulin-receptor will phosphorylate _________

A

IRS-1 (adaptor protein)

39
Q

p-IRS-1 will activate __________in lipid signaling

A

will activate PI3 Kinase to cause formation of PIP3

40
Q

PIP3 will cause activation of kinases such as______ and _____

A

PDK1 and AKT

41
Q

Lipid signaling is responsible for

A

relocalization of GLUT4 transporter onto membrane of fat and muscle cells, which increases glucose uptake

42
Q

Insulin resistance will cause what alterations in adipokines

A

adiponectin ↓ and resistin ↑

43
Q

Adiponectin increases

A

insulin sensitivity

44
Q

resistin increases

A

insulin resistance

45
Q

Excess glucose is lost in urine, meaning there is

A

dehydration

46
Q

No transport of glucose means glucose stays in blood; also continuous glycogenolysis and gluconeogenesis

A

hyperglycemia

47
Q

A characteristic feature of diabetes is the LIPID TRIAD:

A

HIGH FAs, HIGH LDL, and LOW HDL

48
Q

Normally, insulin will suppress ___________ and activates _______

A

suppress Hormone Sensitive Lipase and activates Lipoprotein Lipase

49
Q

transfers lipids to adipose for storage

A

Lipoprotein Lipase

50
Q

releases FAs from adipose in starvation

A

Hormone Sensitive Lipase

51
Q

NO INSULIN means continuous release of fats from adipose due to ______ fats travel to the liver and are turned into ______

A

NO INSULIN means continuous release of fats from adipose due to HSL, fats travel to the liver and are turned into VLDL

52
Q

HDL levels will decrease due to loss of

A

Apo-A1

53
Q

Lungs and kidney respond to ACIDOSIS with

A

Kussmaul Breathing

54
Q

Large amounts of FAs causes buildup of Acetyl-CoA in liver and thus __________ formation begins in the liver

A

ketone body

Biochem 4 (8 decks)

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