Lecture 17 Flashcards

(26 cards)

1
Q

What is the NOVA classification system?

A

Categorizes food on the extent to which they are processed

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2
Q

What is the fraction of adult population with prediabetes?

A

1/3 of adult pop

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3
Q

What is the approx. fraction of prediabetics who go on to full diabetes?

A

Up to 70% of prediabetics-> diabetes

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4
Q

What is prediabetes associated with?

A

early forms of kidney disease, retinopathy, and vascular disease

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5
Q

How are the worldwide trends similar to US?

A

Worldwide trends are reflected in US stats

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6
Q

What are the major risk factors for diabetes?

A
  • Age
  • Excess weight
  • Excess added sugar consumption
  • Excess saturated fat and meat consumption
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7
Q

What is the effect of sugar availability on diabetes risk? (economic analysis)

A
  • Study found that every 150 kcal/person/day increase in sugar availability was associated with increased diabetes prevalence by 1.1%
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8
Q

What are the basic features of a glucose tolerance test (GTT)?

A

blood glucose in diabetic and non-diabetic persons after consuming 75 g test load of glucose

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9
Q

What is the nature of glycation that produces HbA-1C?

A
  • a non enzymatic modification of HbA with glucose; through an Amadori rearrangement (amine->ketone) produces HbA-1C
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10
Q

How does measuring HbA-1C helpful for detection of long term glucose?

A
  • The more glucose in the body-> the more HbA-1C (a monotonic relationship)
  • More useful for long term bc more accurate for long term measurement
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11
Q

what are the normal values of fasting glucose? 2hr post GTT? levels? HbA-1C levels?

A

Fasting glucose: <100 mg/dL
2hr GTT: <140 mg/dL
HbA-1C: <5.7 %

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12
Q

what are the diabetes values of fasting glucose? 2hr post GTT? levels? HbA-1C levels?

A

Fasting glucose: >126 mg/dL
2hr GTT: >200 mg/dL
HbA-1C: >6.4%

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13
Q

What is the difference between visceral fat obesity and subcutaneous fat obesity?

A
  • subcutaneous obesity- healthy adipose tissue

- visceral obesity- dysfunctional adipose tissue

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14
Q

Why are both sumo wrestlers and people with lipodystrophy useful about obesity and pathology?

A

Sumo: high adipose, low metabolic problems
Lipodystrophy: no adipose, high metabolic problems
Results: these studies tells us where the fat is and what it’s doing to our biochemistry

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15
Q

What is the role of genetics in T1D and T1D from twin studies?

A

No one “gene” for diabetes, but there are genetic components to both syndromes

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16
Q

What are clinical interventions and options for T1D and T2D?

A

T1D: glucose monitors, insulin injection, and insulin pumps
T2D: meds, insulin, lifestyle therapies, and bariatric surgery (for weight loss)

17
Q

What is the value of CGM (Continuous Glucose Monitor) in diabetes management?

A

CGMs can distinguish between dropping and increasing blood glucose levels (critical for managing blood glucose levels)

18
Q

What drug treatment for T2D reduce liver glucose over-production

19
Q

What drug treatments for T2D reduces insulin resistance?

A

Avandia and Metformin

20
Q

What drug treatments for T2D stimulates insulin production?

A

Sulfonylureas

Incretins

21
Q

What do Incretins (GLP-1, GIP) do?

A
  • Stimulate insulin release
  • Inhibit glucagon release
    result: Lowering of blood glucose
22
Q

What is Avandia?

A

an insulin sensitizer

23
Q

What class of drug is Avandia a member of?

A

Thiazolidinedione

24
Q

How does Avandia act as an insulin sensitizer? What do they bind to?

A

They reduce glucose, fatty acid, and insulin blood concentrations; they work by binding to the peroxisome proliferator-activated receptors (PPARs)

25
What problems are associated with Avandia?
Heart attack- increases risk about 30% | Macular edema- increases risk 130% (destroys retina-> blindness)
26
What effect does bariatric surgery have on obesity and T2D?