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Sigma-Aldrich) was used, while 0.5 M of the endoplasmic reticulum stress inducer thapsigargin (Sigma-Aldrich) was applied to activate SREBP-2, thereby upregulating genes involved in cholesterol biosynthesis and uptake [22]

Linearity of the response was verified in the range 0.05 to 5 M through 3 experiments to be able to measure low passage

In vivo studies with long-acting glucagon analogue suggest that hypoaminoacidaemia could be an important contributing mechanism to the observed increase in energy expenditure with glucagon agonism, but it also leads to enhanced lean mass loss [63]