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Endocrine > Metabolic homeostasis (L11) > Flashcards

Metabolic homeostasis (L11) Flashcards

1
Q

Seven causes of wasting

A 
Trauma
Infection
Burns
Malnutrition/starvation
Cancer
Psychological
Drug abuse
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2
Q

Daily brain glucose requirement

A

180g

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3
Q

Initial source of glucose during starvation

A

Endogenous fatty acid lipolysis (80%), protein degradation, and breakdown of liver glycogen

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4
Q

Metabolic switch

A

Ketone bodies are used for brain energy supply

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5
Q

How much protein is broken down in prolonged fasted state?

A

Only 20g/day

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6
Q

Waist-hip ratios with increased cardiovascular problems

A

Greater than 0.95 for men, greater than 0.85 for women

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7
Q

Metabolic syndrome

A

Presence of visceral obesity, hypertension, insulin resistance, and dyslipidemia

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8
Q

Parameters for metabolic syndrome

A

BP > 135/80
HDL 150 mg/dL
Waist > 40 in (men) or 35 in (women)
Fasting glucose > 100 mg/dL

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9
Q

Primary hormone in white adipose tissue

A

Leptin

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10
Q

Important transcription factors for leptin

A

SREBP-1 and PPAR-gamma

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11
Q

What does SREBP-1 do?

A

Promotes triglyceride synthesis

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12
Q

What does PPAR-gamma do?

A

Regulates triglyceride storage and adipocyte differentiation

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13
Q

PPAR-gamma agonists

A

Thiazoladinediones; help in treatment of insulin resistance

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14
Q

Side effect of PPAR-gamma agonists

A

Weight gain - clinical consideration

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15
Q

Relationship between total fat and leptin concentrations

A

More body fat correlates with higher leptin levels, but cells become resistant to its effects

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16
Q

Hypothalamic stimulators of appetite

A

Neuropeptide Y, agouti-related protein,

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17
Q

Hypothalamic inhibitors of appetite

A

alpha-MSH, cocaine-amphetamine related transcript (CART)

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18
Q

Process of insulin resistance

A

Slow; constant high levels of blood insulin levels will downregulate the number of insulin receptors and eventually less insulin is made

19
Q

Conversion of type I diabetes to type II diabetes

A

Beta cell “exhaustion” that leads to complete lack of insulin production

20
Q

Elevated HbA1C in diabetics

A

> 6.5%

21
Q

Fasting glucose in diabetes vs prediabetes

A

100-125: prediabetic

126+: diabetic

22
Q

Oral glucose tolerance test

A

Glucose measured after an 8 hour fast, then 2 hours after a 75g consumption of glucose

23
Q

Parameters of oral glucose tolerance test

A

140-199 mg/dL: prediabetic

200+: diabetic

24
Q

Symptoms of DMII

A

Polyphagia, polydipsia, and polyuria

25
Q

Biguanides

A

Metformin: inhibits hepatic gluconeogenesis, increases insulin receptor activity, making cells more sensitive to insulin

26
Q

Alpha-glucosidase inhibitors

A

Delays intestinal absorption of carbohydrates

27
Q

Proposed mechanism of beta cell dysfunction in DMII (7)

A 
Glucose/lipid toxicity
Amyloid buildup
ER stress
Oxidative stress
Reduced expression of beta cell genes
Decreased incretins
Islet inflammation
28
Q

Diabetes mellitus type I

A

Characterized by a juvenile onset and ketoacidosis in the absence of insulin treatment.

29
Q

Prevalence of DMI

A

2-5% of diabetes cases

30
Q

Etiology of ketoacidosis

A

Lack of insulin and increased counterregulatory hormones, increasing fatty acid oxidation and acidosis

31
Q

What happens if ketoacidosis is not treated?

A

Results in acidosis, severe dehydration, and diabetic coma

32
Q

Complications of DM

A

Renal failure

33
Q

Partial vs. absolute insulin deficiency

A

In the presence of some insulin, there will be no ketone formation; only occurs in the complete lack of insulin

34
Q

Plasma osmolality in relationship to mental state

A

Severe dehydration that accompanies a hyperglycemic hyperosmotic state will result in altered mental status

35
Q

Risk factors for DMII

A

Genetic predisposition and environment

36
Q

Gene actions affected in genetic predisposition for DMII

A

Most affect proliferation/differentiation/survival of beta cells, but some affect insulin signaling, glucose transport, or obesity

37
Q

Genes affected in DMII

A

TCF72: Wnt pathway, coactivator of beta-catenin

38
Q

What are the two environmental factors that predispose to DMII development?

A

Impaired beta-cell proliferation during childhood; increased propensity for insulin resistance

39
Q

What factors during childhood will predispose to DMII?

A

Maternal factors during pregnancy; malnutrition

40
Q

Key early characteristic for DMII

A

Impaired rapid release of insulin

41
Q

Islet cell development

A

Islet neogenesis: embryonic devlopment

Beta cell proliferation continues throughout childhood, but is stable in adults

42
Q

Genes important in islet cell development

A

PDX-1: islet cell differentiation and beta cell proliferation
TCF72: downstreat targets regulate beta cell proliferation

43
Q

Exenatide

A

GLP-1 agonist: incretin mimetic that helps improve second phase insulin release

44
Q

Clinical considerations for exenatide

A

May cause pancreatic toxicity (2013)

Endocrine (11 decks)

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