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Metabolism 2 PBL > PBL 4 > Flashcards

PBL 4 Flashcards

1
Q

what causes metabolic syndrome

A
  • low HDL cholesterol
  • visceral obesity
  • insulin resistance
  • hypertension
  • high triglycerides
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2
Q

why is obesity and type 2 diabetes linked

A

Obese individuals have more adipose tissue which increases the amount of
adipokines that are released.

Adipokines can be inflammatory and therefore initiate insulin resistance in
adipocytes

there can be increased macrophage infiltration of the adipose tissue which will further increase the basal level of adipose inflammation and exacerbate inulin resistance

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3
Q

what is obesity associated with

A
  • it is associated with an increase in the number of free fatty acids in the blood stream
  • free fatty acids can increase the synthesis of diacylglycerol and this can cause diacylglycerol induced activation of protein kinase C isoforms
  • PKC can phosphorylate serine and threonine residues on IRS which prevents the phosphorylation of tyrosine on the IRS, AKT is therefore not produced
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4
Q

what is the difference between visceral fat and subcutaneous fat

A
  • Visceral fat - this is a high degree of fatty tissue within the abdomen
  • visceral adipose cells also produce signifiant amounts of pro inflammatory cytokines such as TNF-a and IL-1 and IL-6
  • also linked to NAFLD
  • Subcutaneous fat - distinct from subcutaneous adiposity or fat between the skin and the muscle wall especially elsewhere on the body such as the hips or thighs
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5
Q

what do visceral adipose cells produce

A

Unlike subcutaneous adipose tissue, visceral adipose cells produce significant amounts of proinflammatory cytokinessuch as tumour necrosis factor-alpha andinterleukins -1 and -6, etc.

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6
Q

what do pro inflammatory cytokines do

A

these proinflammatory cytokines disrupt normal insulin action in fat and muscle cells, and may be a major factor in causing the whole-body insulin resistance observed in patients with visceral adiposity.

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7
Q

what is visceral adiposity also linked to

A

Visceral adiposity is related to an accumulation of fat in the liver, a condition known asnon-alcoholic fatty liver disease(NAFLD).

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8
Q

what is the result of NALFD

A

The result of NAFLD is an excessive release of free fatty acids into the bloodstream (due to increased lipolysis), and an increase in hepatic glycogenolysis and hepatic glucose production, both of which have the effect of exacerbating peripheral insulin resistance and increasing the likelihood oftype 2 diabetes.

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9
Q

what things happen in order to get type 2 diabetes with obesity

A

1) increased production of adipokines/cytokines, including tumor necrosis factor-α, resistin, and retinol-binding protein 4, that contribute to insulin resistance as well as reduced levels of adiponectin
2) ectopic fat deposition, particularly in the liver and perhaps also in skeletal muscle, and the dysmetabolic sequelae

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10
Q

how does metformin work

A

This is a biguanide.

  1. Decreases hepatic gluconeogenesis primarily by a transient reduction in activity of the mitochondrial respiratory-chain complex 1.
  2. Metformin also increases glucose uptake in skeletal muscle via GLUT4.
  3. increases GLP-1 reducing blood glucose in muscles
    - only effective if you have pancreatic B cells
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11
Q

how does gliclazide work

A

This is a type of sulfonylurea which attaches to the ATP dependent potassium pump and reduces potassium outflow in beta pancreatic cells. This depolarises cell membrane and activates voltage dependent calcium channels which allows for vesicle fusion and release.

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12
Q

how does pioglitazone work

A
  • This is a type of thiazolidinedione (TZD) which is used to increase sensitivity to insulin.
  • TZDs act by activatingPPARs(peroxisome proliferator-activated receptors), a group ofnuclear receptors, with greatest agonist specificity forPPAR-gamma, PPARG. The endogenousligandsfor these receptors are (FFAs).
  • make you gain weight - our person is trying to loose weight
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13
Q

how does sitagliptin work

A

– This will competitively inhibit the enzyme dipeptidyl peptidase 4 which breaks down GLP-1 and GIP – the gastrointestinal hormones released after eating which increase the release of insulin and also induce satiety.

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14
Q

why does he need insulin injections

A

The insulin resistance will result in compensation by the pancreas which will increase the beta cell mass.

However, this hyperinsulinemia will further exacerbate the resistance (desensitisation).

Eventually, the beta cells undergo decompensation as the cells are unable to maintain their secretion of insulin.

The beta cells begin to die. It is the loss of functional insulin producing beta cells which necessitates insulin injections

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15
Q

what does HbA1c measure

A

Hba1c – a measure of haemoglobin glycosylation

When blood glucose concentration is high, the glucose will covalently bond with the protein haemoglobin

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16
Q

what is HbA1c a measure of

A

HbA1Cis a measure of your average blood glucoselevelover3 months. YourHbA1C target should be under 48mmol/mol (6.5% of total RBC).

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17
Q

what is acanthuses nigricans

A

Dry, rough, thick and velvety patches on the skin, especially near skin folds such as the neck,armpit, around the groin and sometimes in other skin folds

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18
Q

what is acanthuses nigricans a sign of

A

Is a clinical sign of hyperinsulinemia – the insulin will bind to and stimulate insulin receptors and growth-factor 1 receptors on keratinocytes and dermal fibroblasts

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19
Q

why does Addisons disease happen

A

This occurs becausemelanocyte stimulation hormone (MSH) and ACTH share the same precursor molecule, pro-opiomelancortin (POMC).

After production in theanterior pit. gland, POMC gets cleaved into gamma-MSH, ACTH, andbeta ipotropin.

The subunit ACTH undergoes further cleavage to produce alpha-MSH, the most important MSH for skin pigmentation

20
Q

what is nocutira

A
  • urination at night
21
Q

how is glucose reabsorbed

A
  • Once inside the epithelial cells, glucose re-enters the bloodstream through facilitated diffusion throughGLUT2transporters.
22
Q

what is PPARG

A

PEROXISOME PROLIFERATOR – ACTIVATED RECEPTOR GAMMA (PPARG

23
Q

what does PPARG do

A

A nuclear receptor

A transcription factor

Stimulates adipocyte differentiation – stimulating lipogenesis and lipid / FFA uptake - greater risk of type 2 diabetes due to obesity

24
Q

what does GKRP stand for

A

GLUCOKINASE REGULATORY PROTEIN

25
Q

what does GKRP do

A

This regulates glucokinase in the liver

This enzyme will phosphorylate glucose and is the first part of the glycogenesis pathway.

When blood glucose and insulin is low, the GKRP will bind to GK and render it inactive which retains it in the nucleus

When blood glucose (and insulin) and high, the GKRP will allow the GK to translocate into the cytoplasm of the hepatocyte which initiates the first part of glycogenesis.

26
Q

what hormones are appetite stimulating

A

Orexigenic appetite stimulating
– NPY
– AgRP
– MCH

  • gherlin
27
Q

what hormones are appetite inhibiting

A

Anorexigenic appetite inhibiting
– POMC
– CART

  • PYY, leptin, inulin, CCK, GLP-1, 5-HT
28
Q

what is the arcuate nucleus

A

• Main centre for appetite regulation in the hypothalamus

29
Q

what two systems does the arcuate nucleus act by

A

– NPY/Agouti related peptide

– Cocaine related transcript & proopiomelanocortin

30
Q

what does 5-HT do

A

Serotonin in vertebrates is an anorexigenic molecule acting through two receptors, Htr1b and HTr2c – these interact with the ARC

  • Act to increase signalling from POMC neurons [HTr2C]
  • Act to decrease AgRP neuron signalling [HTr1B]
31
Q

what does ghrelin do

A

Ghrelin receptors found on NPY neurons

Secreted from the stomach

Acts to stimulate NPY and thus increase food intake

32
Q

how does GLP-1 and PYY act

A

GLP-1
Glucagon like peptide is released by the L cells of the large intestine at the distal end of the ileum and colon
Interacts to inhibit NpY and stimulate PoMC

PYY
Acts in a similar way to inhibit NpY and stimulate PoMC
Acts on the Y2R receptor

33
Q

how do leptin and insulin act

A

Both leptin and insulin drop AGRP levels

34
Q

how does malonyl CoA work

A

During periods of fasting, hypothalamic levels of malonyl-CoA rapidly decrease and act as a signal of hunger.

Conversely, during feeding, hypothalamic levels of malonyl-CoA rapidly rise and act as a signal to stop eating.

Link back to Fatty Acid metabolism
Level of Malonyl CoA controlled by AMPK

35
Q

what is malonyl CoA controlled by

A

AMPK

36
Q

what is bariatric surgery for

A

For morbid obesity > 40 BMI where pharmacological treatment has failed

37
Q

name some bariatric surgery types

A

1) Restrictive procedures – like gastric binding
2) Malabsorptive procedures – biliopancreatic diversion

and both

38
Q

HbA1c

A

Glycosylated haemoglobin

- measurement for average glucose over 3 months

39
Q

Go2TD research

A

trying to find out what variants are causing diabetes

40
Q

risk factors for type two diabetes

A

Obesity
Family history – first generation, lean otherwise healthy relatives often develop skeletal muscle insulin resistance
Age – increased mitochondrial dysfunction, inflammation
Ethnicity
Increased in incidence follows the trend of urbanisation and lifestyle changes suggesting environmental influences

41
Q

why does everyone who is obese is not type 2 diabetes

A
  • In the normal condition that the pancreas can adjust to the insulin resistance and the islets increase in both size and number due to beta cell increase in size and number
  • New beta cells can be generated – they increase in size and thus produce new insulin or the beta cells can increase in number
  • Increased beta cell function – can increase insulin better
42
Q

How to diagnose type 2 diabetes

A

One abnormal plasma glucose
- (random ≥11.1 mmol/L or fasting ≥7 mmol/L) in the presence of symptoms (thirst, increased urination, recurrent infections, weight loss, drowsiness and coma)
- Two fasting venous plasma glucose samples in the abnormal range
(≥7 mmol/L) recommended in asymptomatic people

Oral glucose tolerance test
- Patient is asked to fast for 8 hours and then they are given a sugary drink, then measure the glucose levels fasting

HbA1c
• Advantages: reliable measure; HbA1c levels are relatively stable vs glucose; ease of sample collection; patient convenience (no need for 8 h fast)
• Limitations: cost in some parts of the world; influence of Hb traits (e.g. HbS, HbF); conditions affecting rbc turnover
• An HbA1c of 48 mmol/mol (6.5%) is recommended as the cut point for diagnosing diabetes
• Currently insufficient evidence to make any formal recommendation on the interpretation of HbA1c levels below this level
• Haemoglobin is glycated

43
Q

What does GLP-1 do

A
  • Increase the glucose induced insulin secretion
  • Inhibits glucagon secretion and hepatic glucose production
  • Slows gastric emptying
  • Promotes satiety
  • In the context of obesity, it slows gastric emptying and gives a longer sense of satiety
  • There are some drugs that act as agonist of the GLP-1 receptor
44
Q

Signs and symptoms of diabetes for type 2

A 
 Weight loss.
 Polyuria (increased urination).
 Polydipsia (increased thirst).
 Polyphagia (increased hunger).
 Blurred vision.
 Headaches.
 Fatigue.
 Nausea and vomiting.
45
Q

Signs and symptoms for type 1 diabetes

A

 Glycosuria.
 Polyuria and dehydrations (due to osmotic diuresis).
- Osmotic diuresis occurs when glucose is present in the kidney tubules and is not
reabsorbed.
- This pulls water back into the tubules and it is excreted.
 Weight loss.
- Weight loss occurs due to loss of glucose in the urine.
 Fatigue.
 Diabetic ketoacidosis.

46
Q

gastric band or balloon and pregnancy

A
  • deflate the balloon and the band - can cause perforation of the stomach and malnutrition which is bad for pregnancy - e..g folic acid deficiency can lead to neural tube defect
47
Q

Name the pill for weight loss

A

xx

Metabolism 2 PBL (9 decks)

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