Flip

the images 180 degrees so they look more anatomically correct

Use

a software program to assist with counting of the fluorescently-labelled cells

Use

a software program to change the fluorescently labelled immune cells from green

to red, so that the colour is different to the apoptotic cells

Use

a software program to enhance fluorescently labelled cells so they are easily

visible on the screen

Activating both the GLP-1 and GIP receptors to improve glycaemic control and satiety.

Increasing the incretin effect in the gut while reducing glucose absorption in the jejunum. 

Stimulating POMC neurons to release -MSH while blocking the -endorphin-mediated "brake" on those same neurons. 

Activating

the "Hungry Brain" while simultaneously increasing "Slow

Burn" energy expenditure.

Brown

adipocytes maintain a stable identity derived from Myf5+ progenitors shared

with skeletal muscle, whereas beige adipocytes originate from Myf5– precursors

and exhibit high plasticity, capable of undergoing "browning" via

The "browning" of white adipose tissue is a permanent developmental shift triggered by β3-adrenergic antagonism, which allows Myf5+ progenitors to bypass mitochondrial uncoupling and maximize ATP synthesis during periods of high-fat feeding.

Beige

adipocytes are the primary constitutive thermogenic cells found in the

interscapular depots of infants, while brown adipocytes are inducible cells

recruited in adults via the transdifferentiation of Myf5– myocytes during

chronic cold exposure

Both brown and beige adipocytes originate from Myf5+ mesenchymal stem cells, but they differ in that BAT is constitutively thermogenic while beige cells require the ectopic expression of the Myf5 gene to maintain UCP1 activity.

Deletion

of POMC cells in the ARC leads to starvation and death due to the loss of

energy-balancing signals.

AgRP is an endogenous antagonist of the MC4R, effectively blocking the anorexigenic effect of α-MSH to induce appetite. 

AgRP

acts as a potent agonist for the MC4R, mimicking the satiety effects of α-MSH.

POMC neurons provide rapid, millisecond-scale control of meal termination via glutamate release. 

The resection of much of the stomach, which significantly reduces ghrelin-producing cells and alters gut peptide secretion (increased GLP-1/PYY).

The

insertion of a silicone band that slows gastric emptying and reduces

postprandial insulin spikes.

It

relies entirely on the secondary effects of weight loss and has no immediate

impact on incretin secretion.

A

massive reduction in ghrelin levels that persists for years.

The

complete inhibition of hepatic gluconeogenesis to save protein stores.

Increased

fatty acid oxidation and the production of ketones, which can cross the BBB and

shift the balance of GABA and glutamate.

The

activation of the parasympathetic nervous system to slow metabolism.

Lipotoxicity

increases the concentration of ceramides in myocytes, ceramides inhibit insulin

signalling by directly blocking the phosphorylation of IRS-1

Lipotoxicity

leads to increased levels of long-chain fatty acids, the ceramides and

diacylglycerols (DAGs) because of partial oxidation of fatty acids, which in

turn interfere with insulin signalling

Lipotoxicity

leads to increased production of short-chain fatty acids, the ceramides and

diacylglycerols (DAGs) because of complete oxidation of fatty acids, which in

turn interfere with insulin signalling

Lipotoxicity

increases the concentration of diacylglycerides (DAGs) in myocytes, DAGs

inhibit insulin signalling by directly blocking the phosphorylation of Akt

Reduced energy expenditure via a reduction in physical activity and reduced ‘browning’ of white adipose tissue leads to increased adiposity

Over-expression

of the FTO gene in mice increases ‘browning’ of white adipose tissue depots,

which leads to increased adiposity

Increased

food intake without any observable changes in food preference, which leads to

weight gain

FTO over-expression increases intake of highly caloric foods without an associated change in energy expenditure, leading to increased fat mass

Pharmaceutical companies

National Health and Medical Research Council (NHMRC)

Philanthropic agencies

State and Territory governments