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Therapeutics II > Diabetes Hockerman > Flashcards

Diabetes Hockerman Flashcards

1
Q

Three Ps of diabetes

A

Polydipsia, polyuria, polyphagia

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2
Q

Mean age of T1DM diagnosis

A

12

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3
Q

How is type 1 diabetes characterized

A

-Autoimmune response that specifically targets pancreatic cells
-Glucose intolerance
-No functioning insulin-secreting pancreatic beta cells
-Dependency on insulin and a tendency towards ketoacidosis
-Family history is often negative

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4
Q

What percentage of beta cell mass must be lost in order for fasting blood glucose to increase from normal levels?

A

~70%

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5
Q

Which autoantigen is present in 99% of type 1 diabetics?

A

islet antigen 2 (IA-2)

57% of non-diabetics who have this antigen will develop type 1 diabetes

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6
Q

Consequences of lack of insulin

A

-Hyperglycemia - Decreased glucose uptake in cells where glucose uptake is insulin-dependent, decreased glycogen synthesis, increased conversion of amino acids to glucose
-Glucosuria - due to high blood glucose
-Hyperlipidemia - increased fatty acid mobilization from fat cells, increased fatty acid oxidation - ketoacidosis
-Uninhibited glucagon - increased glucagon levels in the presence of increased blood glucose levels

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7
Q

Complications caused by diabetes

A

-Cardiovascular - micro and macro angiopathies
-Neuropathy - increased blood glucose levels lead to increased utilization of the polyol pathway (aldose reductase), water accumulation in neurons/reduced protection from oxidative damage
-Nephropathy - renal vascular changes and changes in the glomerular basement membrane
-Ocular - cataracts, retinal microaneurysms and hemorrhage
-Increased susceptibility to infections

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8
Q

Current insulin therapy goals

A

-Keep average blood glucose levels below 150 mg/dL
-Prevent/delay onset of complications
-Increased risk of hypoglycemia

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9
Q

How does hyperglycemia covalently modify proteins?

A

Oxidation products of glucose react irreversibly with proteins to form advanced glycation end-products (AGE)

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10
Q

Complications caused by AGE

A

-Loss of normal protein function
-Acceleration of the aging process
-Theorized to account for many long-term complications of diabetes

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11
Q

Percentage of type 2 diabetics that are obese

A

80%

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12
Q

The typical age of onset for obese type 2 diabetics

A

Usually over 35

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13
Q

The typical age of onset for non-obese type 2 diabetics

A

-Often under 25
-Maturity onset diabetes of the young (MODY)

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14
Q

Cause of non-obese type 2 diabetes

A

Mutations in specific proteins

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15
Q

Cause of obese type 2 diabetes

A

Insulin resistance/decreased BCM

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16
Q

Mechanisms of cell damage initiated by hyperglycemia

A

-Polyol pathway
-Hexosamine pathway
-Protein kinase C pathway
-AGE pathway

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17
Q

Role of alpha subunits

A

-The regulatory unit of the receptor represses the catalytic activity of the beta subunit
-Repression is relieved by insulin binding

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18
Q

Role of beta subunits

A

-Contain the tyrosine kinase catalytic domains
-Autophosphorylation

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19
Q

How does the insulin membrane receptor stimulate glycolysis, glucose uptake, and lipogenesis?

A

-The receptor phosphorylates PI3K which activates PKB causing induction of glycolysis
-PI3K also converts PIP2 to PIP3 which recruits PDK1 also resulting in glycolysis

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20
Q

How does the insulin membrane receptor stimulate glucose uptake?

A

PI3K converts PIP2 to PIP3 which recruits PDK1 which is then able to activate aPKC which stimulates GLUT4 causing glucose uptake into skeletal muscles

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21
Q

How does the insulin membrane receptor stimulate lipogenesis and cell growth/proliferation?

A

-Phosphorylation of PI3K induces lipogenesis
-The receptor also activates MAPK which leads to lipogenesis and cell growth/proliferation

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22
Q

Effects of the insulin membrane receptor

A

-Increased glucose uptake
-Increased lipogenesis
-Increased glycolysis
-Increased glycogen synthesis
-Increased DNA + RNA synthesis (Cell growth/proliferation)
-Decreased gluconeogenesis

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23
Q

Insulin effects on the liver

A

Inhibition of:
-Glycogenolysis
-Ketogenesis
-Gluconeogenesis

Stimulation of:
-Glycogen synthesis
-Triglyceride synthesis

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24
Q

Insulin effect on skeletal muscle

A

Stimulation of:
-Glucose transport
-Amino acid transport

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25
Q

Insulin effect on adipose tissue

A

Stimulation of:
-Triglyceride storage
-Glucose transport

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26
Q

Characteristics of GLUT1

A

-Km 1-2
-Constitutive
-Widely expressed in beta cells

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27
Q

Characteristics of GLUT2

A

-Km 15-20
-Most predominant of the glucose transporters
-Constitutive
-Expressed in beta cells and liver

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28
Q

Characteristics of GLUT3

A

-Km <1
-Constitutive
-Expressed in neurons

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29
Q

Characteristics of GLUT4

A

-Km 5
-Insulin-induced
-Expressed in skeletal muscles and adipocytes

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30
Q

Actions of glucagon

A

-Stimulates glycogen breakdown
-Increases blood glucose

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31
Q

Actions of somatostatin

A

General inhibitor of secretion

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32
Q

Actions of insulin

A

Stimulates uptake and utilization of glucose

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33
Q

Actions of amylin

A

-Co-secreted with insulin
-Slows gastric emptying (slows absorption of glucose)
-Decreases food intake (makes you feel full)
-Inhibits glucagon secretion

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34
Q

How is insulin processed?

A

-Synthesized as a single peptide and deposited in secretory granules
-In secretory granules, is cleaved to A and B chains, and C (connecting) peptide by proconvertases

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35
Q

Lispro (Humalog) onset

A

0.25 hours

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36
Q

Lispro (Humalog) peak

A

0.5-1.5 hours

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37
Q

Lispro (Humalog) duration

A

6-8 hours

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38
Q

Aspart (Novolog) onset

A

0.25 hours

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39
Q

Aspart (Novolog) peak

A

1-3 hours

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40
Q

Aspart (Novolog) duration

A

3-5 hours

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41
Q

Glulisine (Apidra) onset

A

0.25 hours

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42
Q

Glulisine (Apidra) peak

A

0.5-1.5 hours

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43
Q

Glulisine (Apidra) duration

A

3-5 hours

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44
Q

Ultra rapid onset/very short action insulin

A

Lispro (Humalog), Aspart (Novolog), Glulisine (Apidra)

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45
Q

Rapid onset/short action insulin

A

Regular (R)

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46
Q

Regular insulin onset

A

0.5-1 hour

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47
Q

Regular insulin peak

A

2-4 hours

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48
Q

Regular insulin duration

A

8-12 hours

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49
Q

Intermediate onset/action insulin

A

NPH (N)

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50
Q

NPH onset

A

1-1.5 hours

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51
Q

NPH peak

A

4-12 hours (has very clear peak)

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52
Q

NPH duration

A

24 hours

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53
Q

Slow onset/long action insulin

A

Glargine (Lantus), Detemir (Levemir), Degludec (Tresiba)

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54
Q

Glargine (Lantus) onset

A

1-1.5 hours

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55
Q

Glargine (Lantus) peak

A

5 hours

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56
Q

Glargine (Lantus) duration

A

> 24 hours

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57
Q

Detemir (Levemir) onset

A

1-2 hours

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58
Q

Detemir (Levemir) peak

A

4-9 hours

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59
Q

Detemir (Levemir) duration

A

> 24 hours

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60
Q

Degludec (Tresiba) onset

A

1 hour

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61
Q

Degludec (Tresiba) peak

A

9 hours

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62
Q

Degludec (Tresiba) duration

A

> 24 hours

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63
Q

Mechanism of action for NPH insulin

A

Insulins are bound to a protamine. Protamine is then dissolved by tissue proteases releasing free insulin. This results in a slow absorption and a long duration of action.

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64
Q

Characteristics of Lispro (Humalog)

A

-Reversing positions of P28 and K29 on insulin B chain results in decreased self-association (no hexamer formation)
-Place in insulin therapy - injected immediately before meals

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65
Q

Characteristics of Aspart (Novolog)

A

-Proline 28 in B chain is changed to Aspartate (disrupts dimerization)
-Injected immediately before meals

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66
Q

Characteristics of Glulisine (Apidra)

A

-Asn 3 and Lys 29 in B chain are switched to Lys and Glu
-Inject immediately before meals

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67
Q

Characteristics of Glargine (Lantus)

A

-Asn 21 of a-chain is changed to Gly
-2 Arg residues added to the end of the b-chain (30 and 31)
-Clear solution at pH of ~ 4.0: precipitates when neutralized
-Once daily injection
-No pronounced peak

68
Q

Characteristics of Detemir (Levemir)

A

-Thr 30 of b-chain is deleted, and Lys 29 is myristylated (fatty acid attached)
-Binds serum albumin extensively (due to fatty acid)
-Injected once or twice daily

69
Q

Characteristics of Degludec (Tresiba)

A

-Thr 30 of b-chain is replaced by gamma-Glu/C16 fatty acid
-Binds serum albumin extensively (due to fatty acid)
-Injected once daily

70
Q

Common multi-dose insulin regimens

A

-Fast onset, short acting taken before meals
-Long, or intermediate taken at bedtime or at bed time and after breakfast

71
Q

Common insulin mixture formulations

A

NPH + regular:
-Humulin 70/30
-Humulin 50/50

NPL (neutral protamine lispro) + Lispro
-Humalog 75/25
-Humalog 50/50

Ryzodeg (70% Degludec + 30% Aspart)

These give a transient preprandial bolus and a prolonged basal level in a single injection

72
Q

Characteristics of Afrezza

A

-Regular Human Insulin in a dry powder inhalation
-Rapid onset, shorter duration of action the subq injection - used as pre-prandial insulin

73
Q

What is Afrezza contraindicated in?

A

-Contraindicated in patients with asthma and COPD
-May reduce lung function (decreased FEV)

74
Q

Routes of administration for insulin

A

-Subcutaneous - all preparations
-Insulin infusion pump - Buffered Regular also rapidly acting insulins
-IV - Regular (for severe hyperglycemia or ketoacidosis)
-Inhalation - Afrezza

75
Q

Types of patients that use insulin

A

-Type 1 diabetics
-Patients with ketosis and hyperosmolar coma
-Some type 2 diabetics

76
Q

What is the main adverse reactions to insulin?

A

-Hypoglycemia - blood glucose <60 mg/dL
-Lipodystrophy - lump of fat at over used injection site
-Lipohypertrophy - accumulation of fat in subcutaneous tissue
-Lipoatrophy - concavities in subcutaneous tissue
-Antibodies can be formed against insulin from insulin therapy

77
Q

How to treat hypoglycemia?

A

Glucose or glucagon

78
Q

What can cause hypoglycemia?

A

Too much insulin or not enough food

79
Q

Agents that can increase blood glucose (especially in diabetics)

A

-Catecholamines
-Glucocorticoids
-Oral contraceptives
-Thyroid hormone
-Calcitonin
-Somatropin
-Isoniazid
-Phenothiazines
-Morphine

80
Q

Agents that may increase the risk of insulin hypoglycemia

A

-Ethanol (#1 cause)
-ACE inhibitors
-Fluoxetine
-Somatostatin
-Anabolic steroids
-MAO inhibitors
-beta adrenergic blockers
-Vigorous, unaccustomed exercise

81
Q

Treatment plan for T1DM

A

Insulin + diet + exercise

82
Q

Treatment plan for T2DM

A

-Diet + exercise
-Diet + exercise + antidiabetic drugs
-Diet + exercise + insulin

83
Q

Agents that enhance insulin secretion

A

Sulfonylureas and meglitinides

84
Q

Examples of meglitinides

A

-Nateglinide
-Repaglinide

85
Q

Why do sulfonylureas only work in T2DM?

A

Must have functioning beta cells

86
Q

Function of sulfonylureas

A

-Restore first phase insulin release
-Increase beta cell sensitivity to glucose and increase glucose stimulated insulin release

87
Q

Effects of sulfonylureas on beta cell insulin release

A

-Binds to sulfonylurea receptors
-Inactivates K+ channel
-Decreased cell polarization
-Activates voltage sensitive Ca+ channels
-Increase Cai++ and activity of microfilaments
-Increased exocytosis of insulin containing granules

88
Q

Pharmacophore of sulfonylureas

A

Sulfonylurea group (im not paying for premium look it up for image)

89
Q

Tolbutamide (Orinase) potency

A

1

90
Q

Tolbutamide (Orinase) Duration

A

6-12 hours

91
Q

Tolazamide (Tolinase) potency

A

5

92
Q

Tolazamide (Tolinase) duration

A

12-14 hours

93
Q

Chlorpropamide (Diabinese) potency

A

6

94
Q

Chlorpropamide (Diabinese) duration

A

14-72 hours

95
Q

Glipizide (Glucotrol) potency

A

100

96
Q

Glipizide (Glucotrol) duration

A

12-24 hours

97
Q

Glyburide or Glibenclamide (DiaBeta, Glynase) potency

A

150

98
Q

Glyburide or Glibenclamide (DiaBeta, Glynase) duration

A

24 hours

99
Q

Glimepiride (Amaryl) potency

A

~150

100
Q

Glimepiride (Amaryl) duration

A

24

101
Q

First generation sulfonylureas

A

Tolbutamide, Tolazamide, Chlorpropamide

102
Q

Second generation sulfonylureas

A

Glipizide, Glyburide/Glibenclamide, Glimepiride

103
Q

Pharmacophore of meglitinides

A

Phenylalanine group (im not paying for premium look it up for image)

104
Q

What is Repaglinide (Prandin)?

A

A non-sulfonylurea hypoglycemic agent (Glinide)

105
Q

Repaglinide (Prandin) mechanism of action

A

Like sulfonylureas

106
Q

Repaglinide (Prandin) onset

A

-Quick onset with short duration of action (t1/2 - 1 hour)
-Take tablet before meal

107
Q

Characteristics of Nateglinide (Starlix)

A

-Non-sulfonylurea KATP channel blocker (Glinide)
-Very specific for KATP channels in pancreas vs CV tissue
-Shorter half-life than Prandin so less risk of hypoglycemia
-Synergistic with metformin

108
Q

Possible adverse events from sulfonylureas

A

-Lasting and prolonged hypoglycemia (due to long half life) (this has been misdiagnosed as stroke)
-Risk of cardiovascular events/mortality?
-GI problems
-Weight gain and increased numbers of secondary failures (can see a decreased ability to make insulin because of the stress on beta cells)

109
Q

Drug interactions with sulfonylureas

A

-Salicylates
-Phenylbutazone
-Sulfonamides
-Clofibrate
-Oral contraceptives
-Corticosteroids
-Epinephrine
-Thiazide diuretics
-Corticosteroids
-Thyroid

110
Q

Agents that enhance the incretin effect

A

-GLP-1R agonists
-GLP-1 and GIP dual agonist
-DPP-IV inhibitors
-Amylin analogs

111
Q

What is the incretin effect?

A

Oral glucose stimulates a larger insulin response than IV glucose in humans because of receptors in the intestines that bind to glucose and result in insulin secretion

112
Q

Benefits of GLP-1 agonists

A

-Reduce hyperglycemia with low risk of hypoglycemia
-Weight loss
-Increase beta cell mass

113
Q

Example of GLP-1 agonists

A

Exenatide (Exendin 4; Byetta), Liraglutide (Victoza), Dulaglutide (Trulicity), Lixisenatide (Adlyxin), Semaglutide (Ozempic), Semaglutide oral (Rybelsus)

114
Q

Warnings for all GLP-1 analogs

A

-Nausea and vomiting
-Pancreatitis
-Risk of thyroid C-cell tumors
-Contraindicated in patients with a family history of medullary thyroid cancer

115
Q

Characteristics of Exenatide (Exendin 4; Byetta)

A

-Activates GLP-1 receptor
-Enhances first phase secretion
-Longer half-life than GLP-1
-Twice daily injections or once per week injections (Bydureon)
-Can be co-administered with metformin, TzDs, or sulfonylureas

116
Q

Characteristics of Liraglutide (Victoza)

A

-GLP-1analog
-Half-life of 13 hours
-Subq daily
-Can be co-administered with metformin, TzDs, and sulfonylureas
-Monitor calcitonin levels

117
Q

Characteristics of Dulaglutide (Trulicity)

A

-GLP-1 agonist
-Injected subq once a week
-GLP-1 agonist peptides are slowly released from IgG Fc domain by reduction of disulfide bonds in linker region

118
Q

Characteristics of Lixisenatide (Adlyxin)

A

-GLP-1 receptor agonist
-Injected subq daily before breakfast

119
Q

Characteristics of Semaglutide (Ozempic)

A

-GLP-1 receptor agonist
-Injected subq once per week
-Extensively bound to serum albumin - t1/2 ~ 1 week

120
Q

Characteristics of Semaglutide oral (Rybelsus)

A

-Orally available GLP-1 receptor agonist
-Oral bioavailabilty - o.4-1.0%
-Absorbed from stomach
-Dosed once daily

121
Q

Characteristics of Mounjaro (Tirzepatide)

A

-Full GIP receptor agonist
-Biased GLP-1 receptor agonist preferential coupling to cAMP over beta-arrestin
-Reduces internalization (desensitization) of GLP-1 receptor to maintain GLP-1 effect
-Weekly subq injection
-Purported to reduce A1c and body weight more effectively than GLP-1 receptor agonists

122
Q

What is Dipeptidyl Peptidase 4 (DPP-4)

A

The enzyme that degrades GLP-1

123
Q

Examples of DPP-4 inhibitors

A

Sitagliptin (Januvia), Saxagliptin (Onglyza), Linagliptin (Tradjenta), Alogliptin (Nesina)

124
Q

Characteristics of DPP-4 inhibitors

A

-Administered orally - once daily
-Reduce hyperglycemia and HgbA1c
-Low risk of hypoglycemia
-Considered weight neutral
-May be co-administered with metformin, TzDs (all are available in combination with metformin)

125
Q

Metabolism and excretion of Januvia and Nesina

A

Not extensively metabolized, excreted in urine (kidney)

126
Q

Metabolism and excretion of Tradjenta

A

Not extensively metabolized, excreted in feces (liver)

127
Q

Metabolism and excretion of Onglyza

A

CYP3A4/5 substrate, major metabolite active, excreted in urine (kidney)

128
Q

Side effects of DPP-4

A

-Nausea
-Vomiting
-Constipation
-Headache
-Severe skin reactions
-Pancreatitis
-Joint pain
-Heart failure
-Reduced white blood cell counts - infections
-Potential increased risk of cancers

129
Q

Characteristics of Pramlintide (Symlin)

A

-Amylin analog
-Normally co-secreted with insulin
-Slows gastric emptying, decreases fluid intake, inhibits glucagon secretion
-Blunts post-meal rise in blood glucose
-Used in conjunction with insulin - increased subq
-Useful in both type 1 and type 2 diabetes

130
Q

Examples of alpha-glucosidase inhibitors

A

Acarbose, Miglitol

131
Q

Examples of SGLT2 inhibitors

A

Canagliflozin, Empagliflozin, Dapagliflozin, Ertugliflozin

132
Q

Mechanism of action of alpha-glucosidase inhibitors

A

Decrease the absorption of carbohydrate from the intestine via inhibition of gut alpha glucosidases

133
Q

Adverse effects of alpha glucosidase inhibitors

A

Both: GI – diarrhea, nausea, flatulence
Acarbose: risk of liver damage at doses > 100mg tid

134
Q

Strategy for SGLT2 inhibition

A

Blocks SGLT2 transporter in the kidney that prevents reuptake of glucose to the blood

135
Q

Pharmacophore of SGLT2 inhibitors

A

Glucose attached

136
Q

Characteristics of SGLT2 inhibitors

A

-Orally active
-Indicated for Type 2 diabetes as an adjunct to diet and exercise
-Decreases A1c as monotherapy with metformin, sulfonylureas
-Significant weight loss observed with monotherapy

137
Q

Warning for SGLT2 inhibitors

A

-Increased risk of genital/UT infections
-Increased urine flow/volume depletion/hypotension
-Increased rusk of diabetic ketoacidosis (DKA)
-Contraindicated in patients with renal impairment
-Increased risk of lower limb amputation

138
Q

Example of biguanide

A

Metformin

139
Q

Examples of thiazoladinediones

A

Pioglitazone, Rosiglitzone

140
Q

Causes of insulin resistance

A

-Polymorphism in insulin signaling pathway proteins (rare)
-Obesity - especially accumulation of fat in the abdominal cavity
-Inactivity

141
Q

Effect of insulin resistance on certain tissue types

A

-Skeletal muscle - impaired glucose uptake
-Adipose tissue - impaired glucose uptake, impaired inhibition of lipolysis, mobilization of FAs to other tissues
-Liver - impaired inhibition of glucose output (via gluconeogenesis or glycogenolysis)

142
Q

Role of fatty acids in obesity-induced insulin resistance

A

-Free fatty acid (FFA) levels are increased in obese
-Acutely raising FFA levels causes insulin resistance (IR)
-Acute lowering of plasma FFA levels reduces chronic IR
The predominant effect is on insulin-stimulated glucose transport

143
Q

What does metformin do?

A

-Classified as an antihyperglycemic agent
-Decreases blood glucose concentrations in T2DM without the concentration falling below normal
-Increases the efficiency or sensitivity to insulin in liver, fat, and muscle cells

144
Q

Advantages of biguanides over sulfonylurea

A

-Rarely causes hypoglycemia
-Rarely causes weight gain

145
Q

Mechanism of action of metformin

A

Activator of AMP-activated kinase (AMPK)

146
Q

What does metformin do in the liver

A

Blocks FBPase which prevents the conversion of fructose-1,6-bisphosphate to fructose-6-phosphate

147
Q

What does metformin do in the liver

A

Promotes GTPase activity of Rab causing it to dissociate from GLUT4 allowing it to stay on the cell surface to transport glucose back into the cell

148
Q

What is metformin contraindicated in?

A

Disorders that increase the tendency toward lactic acidosis

149
Q

Adverse effects of metformin

A

-Decreased vitamin B-12 absorption
-GI discomfort

150
Q

Effects of metformin on blood lipid profile

A

-Decreased serum triglycerides
-Decreased serum LDL
-Reduces risk of adverse cardiovascular

151
Q

Thiazolidinediones mechanism of action

A

-Deccrease insulin resistance or improve target cell response to insulin
-Activators of peroxisome proliferator-activated receptor gamma (PPARgamma), a transcription factor

152
Q

Targets of thiazolidinediones

A

Adipocytes:
-Enhances adipocyte differentiation
-Enhances FFA uptake into subq fat
-reduces serum FFA
-Shifts lipids into fat cells from non-fat cells

Liver:
-Enhances glucose uptake
-Reduces hepatic glucose production

Skeletal muscle:
-Enhances glucose uptake

153
Q

Warnings for thiazolidinediones

A

-Restricted prescribing due to cardiovascular toxicities
-Actos is associated with an increased risk of bladder cancer
-Some hepatotoxicity – check liver function
-Do not cause hypoglycemia
-FDA warning - both are contraindicated in class II or IV heart failure

154
Q

Factors regulated by the activation of PPARgamma

A

-Resistin - Elevated in type 2 diabetes
-Adiponectin - Decreased in type 2 diabetes
-TNFalpha - Increased in type 2 diabetes

155
Q

What is resistin?

A

Stimulates glucose export by liver and insulin resistance

156
Q

What is adiponectin?

A

Reduces blood glucose and insulin resistance

157
Q

What is TNFalpha?

A

Stimulates lipolysis in WAT and insulin resistance

158
Q

What happens to insulin response in early pregnancy

A

Increased insulin response e.g. hypoglycemia in T1D

159
Q

What happens to insulin response in late pregnancy

A

Reduced insulin sensitivity because of growth of fetus

160
Q

What is gestational diabetes

A

-Defined as hyperglycemia during pregnancy during pregnancy in otherwise non-diabetic women
-Diagnosed with 24-28 week OGTT
-Affects 2-10% of pregnancies

161
Q

When does gestational diabetes usually appear?

A

Usually appears around week 24 of gestation - in the rapid growth stage of gestation, after fetus has formed - not associated with defects in fetal development

162
Q

Complications that occur from gestational diabetes

A

-Damage to baby during birth (particularly shoulders)
-Neonatal hypoglycemia
-Breathing problems - high glucose or high insulin levels can delay maturation of lungs
-Increased risk of developing type 2 diabetes

163
Q

Maternal insulin resistance in gestational diabetes mellitus

A

-Inability of target tissue to respond to insulin
-Insulin doesn’t cross the placenta, but glucose!
-Factors secreted by the placenta into the maternal circulation

164
Q

What are the placental hormones suspected in gestational insulin resistance

A

CRH-cortisol:
-Both increase as pregnancy progresses
-Glucocorticoids oppose insulin action

Progesterone:
-Increases as pregnancy progresses

Placental GH (GH-V):
-Released during half of gestation
-May contribute to insulin resistance

Placental lactogens:
-Increases as pregnancy progresses
-85% identical to GH-contributes to insulin resistance

165
Q

GDM is predictive of T2D later in life. Why?

A

Exposes the body’s inability to react to insulin resistance

166
Q

Hormones that increase beta cell mass during pregnancy

A

Prolactin:
-Increases as pregnancy progresses
-Stimulates beta cell proliferation

Placental lactogen:
-Activates PRL (high aff) and GH receptors (low aff)

167
Q

Treatment of gestational diabetes

A

-Diet: small meals, complex carbs, avoid sugary foods
-Insulin : gold standard - doesn’t cross placenta
-Glyburide: works- but may harm fetus
-Metformin: works- crosses placenta but does not harm fetus
-Thiazolidinediones- NOT USED

Therapeutics II (33 decks)

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