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Nutrients & Metabolic Disease > 1 Glucose Sensing > Flashcards

1 Glucose Sensing Flashcards

1
Q

Why is hyperglycaemia dangerous?

A

Releases free radicals primarily through a process called “glucose autoxidation,” where excess glucose in the bloodstream spontaneously reacts with oxygen, resulting in ROS

Diabetic ketoacidosis (DKA) occurs when the body doesn’t have enough insulin to use blood sugar for energy. This causes the body to break down fat instead, which produces ketones.

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2
Q

Where is glucose sensed?

A

Pancreas
Liver
Muscle
Adipose
BRAIN

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3
Q

Why does the brain need so much glucose?

A

Because it cannot store fuel

Could use lactate and fat = not as effficient as glucose

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4
Q

What happens when glucose is low in the periphery?

A

More blood flow is needed to go to the brain

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5
Q

What are key glucose sensing reigons of the brain?

A

Ventral medial hypothalamus (VMH)

Medial amygdala nucleus (MAN)

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6
Q

What is 2-DG?

A

2-deoxyglucose

Glycolysis inhibitor, increases the food intake in rats

Acts as a glucose analog, meaning it mimics glucose but cannot be fully metabolized by the body, effectively inhibiting the glycolysis pathway and restricting energy production within cells, making it a potential anti-cancer agent by starving rapidly dividing cancer cells of energy needed for growth

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7
Q

What are counterregulatory hormones?

A

A group of hormones that work to prevent hypoglycemia and maintain fuel supplies in the body

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8
Q

What happend when 2-DG was injected into the brain locally?

A

This made the brain think it was hypoglycaemic because glycolysis could not continue

The rest of the body was euglycemic but the brain cause an increase of counterreggulatory hormones

These hormones work to prevent hypoglycemia

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9
Q

What happened when the brain was euglycemic but the body was hypoglycemic?

A

Counterregulatory hormones were decreased

This shows that the brain controls glucose sensing and homeostasis

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10
Q

What is glucose clamping?

A

Holding glucose at a set level

Hypo-, eu-, hyperglycamic level

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11
Q

What is VGLUT2?

A

Synaptic vesicular transporters = required for vesicular uptake and, consequently, synaptic release of neurotransmitters

(VGLUTs for glutamate and VGAT for GABA)

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12
Q

What expresses VLUT2?

A

Ventromedial hypothalamic (VMH) neurons are predominantly glutamatergic and express VGLUT2

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13
Q

Where are SF1 neurones found?

A

Major subset of VMH neurons

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14
Q

Why did they generate mice lacking VGLUT2 selectively in SF1 neurons?

A

To evaluate the role of glutamate release from VMH neurons

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15
Q

What happened to mice lacking VGLUT2?

A

Hypoglycemia during fasting

Impaired fasting-induced increases in glucagon (glucose-raising pancreatic hormone)

Defective counterregulatory responses to insulin-induced hypoglycemia and 2-deoxyglucose (an antimetabolite)

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16
Q

Why is glutamate release from VMH neurones important?***

A

Functions to prevent hypoglycemia

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17
Q

Why may hypoglycaemia come about?

A

When insulin acts to decrease blood glucose, if glucagon is not responding = cannot create more glucose in the body

18
Q

Why do mice with VGLUT2 KO need higher rate of glucose infusion durign hypoglycaemia clamp?

A

Because decreased rates of endogenous glucose production

19
Q

What happens when VGLUT2 is KOd?

A

Hypoglycemia induced a large increase in plasma glucagon levels in control mice
This response was undetectable in Sf1-Cre;Vglut2flox/flox mice (Figure 5E).

Similarly, hypoglycemia induced a large increase in blood levels of epinephrine in control mice, and this response was blunted in Sf1-Cre;Vglut2flox/flox mice

These results demonstrate that Sf1-Cre;Vglut2flox/flox mice have an impaired counterregulatory response to insulin-induced hypoglycemia.

20
Q

Why is using 2-DG useful?

A

Not confounded by the presence of hyperinsulinemia, scince it cannot be metabolized

(inhibits glucose metabolism in cells)

21
Q

What is MAN?

A

Medial Amygdala Nucleus

22
Q

How do we know MAN and VMN communicate?

A

Because they share several roles

We can also use retrograde labelling

23
Q

What roles do MAN and VMN share?

A

Body weight control

Ovulation

Sexual Behaviour

Fear / Anxiety behaviours

24
Q

What is retrograde labelling used for?

A

Technique used in neuroscience to identify the cell bodies of neurons that project to a specific target area by injecting a tracer substance into that target area

To determine the location of the cells of origin of a nervous system pathway

25
Q

How does retrograde labelling work?

A

Injecting a tracer substance into a target region of the nervous system

It is then taken up by the synaptic terminals of neurons and transported backwards along the axon to the cell body

(forward = cell body to axon)

26
Q

What does glutamic acid decarboxylate do?

A

Converts glutamate into GABA

27
Q

Where are GABA and its receptors made and expressed?

A

VMH

28
Q

Where is GABA A a3 expressed?

A

GABAA receptor subunit α3 is expressed throughout most of the dorsomedial region

29
Q

Where is GABA A a5 expressed?

A

GABAA receptor subunit α5 is localized to the central region

30
Q

Where is GABA A b2, b3 + g3 expressed?

A

the GABAA receptor subunits β2, β3, γ3 are expressed in the most ventrolateral portions

31
Q

What does muscimol do?

A

Muscimol increases GABA’s affinity for the receptor, which enhances neuronal inhibition and causes a subsequent reduction in pain sensation

32
Q

What does bicuculline do?

A

Bicuculline acts as a competitive antagonist at the GABA receptor, meaning it blocks the action of the neurotransmitter GABA, effectively preventing it from binding to its receptor and causing an excitatory effect, often leading to seizures when administered in research settings

33
Q

How is glutamic acid decarboxylase releated to diabetes?

A

Glutamic acid decarboxylase (GAD) is considered to be one of the strongest candidate autoantigens involved in triggering beta-cell-specific autoimmunity

The body’s immune system mistakenly attacks and destroys pancreatic beta cells that produce insulin, leading to diabetes, because it produces autoantibodies against GAD, which is present in these beta cells

34
Q

What are the two isoforms of GAD?

A

GAD 65 = rapid neurotransmission

GAD 67 = sustained GABA production

35
Q

Where do GABAergic neurones in the MAN directly project?

A

VMN

36
Q

Where are the origins of GABAergic inputs to VMN from?

A

Forebrain

Hindbrain inputs to VMN are non-GABAergic

37
Q

What does an insulin affibody do?

A

Binds and blocks the insulin receptor (instead of activating it)

38
Q

What does Phloridzin do?

A

Phloridzin induces hypoglycemia by acting as a competitive inhibitor of the sodium-glucose cotransporter (SGLT) in the kidneys, which prevents the reabsorption of glucose from the urine, effectively causing the body to excrete more glucose and lowering blood sugar levels

39
Q

How do we know hypothalamus insulin regulates alpha-cell glucagon release under hypoglycaemia?

A

When insulin is blocked and glucose is infused normally glucagon will decrease

But when insulin is blocked

40
Q

What happens to GIR and glucagon when VMH insulin is blocked under insulin-induced hypoglycaemic conditions and why?

A

Glucose infusion rate decreases and glucagon increases

Blockade of insulin action within the VMH reduced by 50%
The GIR required to maintain the same hypoglycemic plateau compared with microinjection of a control affibody
Because insulin was blocked, it seemed there wa

41
Q

What happens to GIR and glucagon when VMH insulin is blocked under phloridzin-induced hypoglycaemic conditions and why?

A

Glucose infusion rate increases and glucagon decreases

Glucagon decreases because insulin levels are still high; this signals to the body that there are still high levels of energy and inhibits glucagon secretion

Nutrients & Metabolic Disease (13 decks)

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