L13*-Absorptive & non-absorptive states Flashcards

(23 cards)

1
Q

Define Absorptive state. another name for the state? and explain the energy metabolism for this state.

A

-Fed state
-Refers to the pattern of energy metabolism due to high concentration of the nutrients in the blood as a result of absorption of the nutrients in the FED state.
-Some of the nutrients are used to meet immediate energy needs while the excess are stored for energy later.

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2
Q

Define post-absorptive state. Another name for the state. and explain the energy metabolism for this state.

A

-Fasted state
-A pattern of energy metabolism adopted between meals or during fasting.
-Changes in pattern of energy metabolism depends on the changes in the blood concentration of insulin and other hormones.

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3
Q

Explain the pathway of nutrients in the absorptive state. and give an example of the pathway of a lipid in absorptive state.

A

-In the absorptive state(fed state), the absorbed nutrients are hexose sugars(glucose, fructose, galactose) and amino acids.
-These nutrients go through the liver into circulation.
-Other nutrients go into adipose tissue, muscles and other tissues.

Lipids > small intestines > lymph (chylomicrons) > venous blood > adipose tissue (not 🧠bc too big)

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4
Q

Explain the control of absorptive state in the activation of insulin from the uptake of glucose.

A

1.Absorptive state :-

Feeding glucose
👇
Uptake of glucose
👇
increase in blood sugar
👇
Glucose > Enters pancreas > GLUT2 > SGLT1>to mitochondria > glycolysis> Krebs cycle > oxidative phosphorylation > increase in ATP

  1. Beta-cells in Islets of Langerhans :-

increase in ATP
👇
causes K+ channels to close
👇
membrane depolarisation
👇
increase in Ca2+ intracellular > insulin exocytosis (Bc Ca2+ helps t get insulin to the vesicles)

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5
Q

Give me a example of a disease where glycogen storage does not work as usual to break down to give glucose.

A

Pompeii disease
-Glycogen is normally synthesised in the liver of 💪s.
-A disorder with glycogen storage cause accumulation of glycogen or change in structure of glycogen.
-An autosomal recessive disorder which affects the functioning of lysosomal acid alpha-glucosidase due to mutation of GAA gene.
👇
causes cellular damage
-In healthy individuals glycogen accumulates in the cytoplasm of liver and 💪 cells. However patients with Pompeii disease have glycogen accumulated in the lysosome of these cells instead.

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6
Q

Describe the details of insulin relating to its function in the absorptive state.

A

-Insulin is a hormone secreted by the pancreas.
-Insulin largely influences the pattern of metabolism observed.
-The release of insulin is stimulated by fed state and inhibited by the fasted state.
-In the fed state, the high [glucose]/[amino acids] in the blood stimulates the release of insulin.
-Hormones and NTMs also influence insulin secretion.

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7
Q

What can we convert excess glucose into in adipose tissue ?

A

Fatty acids and glycerol

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8
Q

Describe the details of insulin relating to its function in the post-absorptive state.

A

-The 🧠 and RBC largely depend on glucose for energy.
-Lack of glucose 👉 brain damage, coma, death
-In the post-absorptive state, plasma levels of glucose is maintained by glucose-supplying and glucose sparing reactions.
-So insulin secretion is impaired (inactivated in the fasted state), the pattern of metabolism = post-absorptive state.
-In this state, glucose can simply get into the tissues(all except 💪&adipose tissues) that ARE NOT insulin dependent tissues.

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9
Q

Name few insulin dependent tissues.

A

💪 and adipose tissues

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10
Q

How is glucose maintained in short term period of time ?

A

via glucose supplying reactions

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11
Q

How is glucose maintained in long term period of time ? for days without eating …

A

Glucose sparing reactions

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12
Q

Describe the steps for ketogenesis.

A

Adipose tissue break down triglycerides into fatty acids and glycerol.
👇
That fatty acids then travel to the liver to produce ketone bodies.
👇
Ketone bodies can act as a source or a precursor source for energy.
👇
another pathway to produce ATP other than glucose.

***Brain and other tissues use ketone bodies as a source of ATP in those glucose sparing reactions( in long term with starvation).

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13
Q

Explain Starvation

A
  • in famine, starvation is prevalent(common).
    -extreme suffering caused by lack of food.
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14
Q

What are the metabolic processes that would have been occurring to enable people to maintain their plasma [glucose] ?

A

-Depletion of Carbohydrate precursors
-Increased gluconeogenesis (a.a ☞ glucose)
-After 48 hrs, energy is supplied by ketone bodies and free fatty acids
-Prolonged starvation initiates catabolism (organ system dysfunction)
-breaking down muscle proteins to produce amino acids when desperate => catabolism

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15
Q

Describe the 2 types of Diabetes mellitus.

A

Type 1
-young onset
-loss of Beta cells
-cannot utilise glucose > other fuels
- weight loss
-insulin 💉
-immune system attacks the pancreas âž¡ little to no insulin production

Type 2
-prevalence , 👆 age
-👆 insulin but resistance
-weight loss, ketoacidosis
-Body becomes resistant to insulin

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16
Q

Describe how Diabetes affects the absorptive and post-absorptive state.

A

For type 1 and 2 Diabetes Mellitus, the insulin receptors are present. However, these receptors are either damaged or not responding to signalling.
Poor management of diabetes affects tissues in the body.

17
Q

What does the [insulin] in the plasma based on ?

A

On the level of plasma glucose.

18
Q

Name few tests for diabetes and how does obese affect this ?

A

-Glucose tolerance test > used to diagnose diabetic states. The test relies on the metabolic pattern in absorptive state.
-Fasting blood sugar test > used to diagnose diabetic states. The test relies on the metabolic pattern in post-absorptive state.
-Obesity causes slower uptake of glucose > insulin resistance > increase in plasma glucose

19
Q

Bc of obese issues, what is considered as a more reliable test for the diagnosis and management of diabetes.

A

Haemoglobin A1C (HbA1C)

20
Q

Name a agonist used for the management of Type 2 Diabetes Mellitus.

A

-Glucagon-like peptide-1 (GLP-1) agonists
-GLP-1 is a peptide produced by the cleavage of proglucagon in pancreatic islet alpha-cells.

GLP-1 activates GLP-1 receptors in the pancreas
👇
increase insulin release(improve insulin release)
👇
decrease glucagon release
👇
decrease gastric emptying

21
Q

Describe glycation

A

-when sugar molecules attach to proteins without the help of enzymes.
-Maillard reaction ( not enzymatic browning)
-this is y food goes brown when cooking to enhance the flavours.
- makes the food taste good.
- here is alters enzymes / protein function
-glycation reaction leads to the formation of AGEs ( Advanced glycation end products). these trigger the expression of cytokines which leads to cancer and diabetic complications.

22
Q

Explain the impact of chronic diabetes in the eyes. -retinopathy

A

-Retinopathy - damage affecting the retina
- growth of poor-quality new blood vessels in the retina.
- Macular oedema
- which can lead to severe vision loss
-Blindness

23
Q

Explain the impact of chronic diabetes to the nerves or legs - Neuropathy

A

-Neuropathy - damage affecting the nerves.
-decreased sensation in hands and feet.
-damages blood vessels
-diabetic foot ulcers
-delayed healing > secondary infection > Amputation