Tesamorelin mastery course
Unit 4 of 11

Preserved pulsatility and the IGF-1 axis

The central pharmacologic argument for tesamorelin is a shape, not a size: it acts on the pituitary rather than…

A pulse the axis still governs, and where the fat goes

The central pharmacologic argument for tesamorelin is a shape, not a size: it acts on the pituitary rather than replacing the hormone, so the feedback loops that govern a natural pulse still apply. Read that as the argument it is. A review and a trial introduction here state that tesamorelin restores pulsatile GH secretion, and the 2014 liver trial found mean overnight GH rose against placebo, but none of the papers behind this course publishes an analysis of the pulse pattern itself. That argument also does not make the rise small: the FDA label reports IGF-1 above 2 standard deviation scores in 47 percent of treated patients at 26 weeks, which is why IGF-1 is monitored rather than assumed safe.

This unit contrasts pulsatile with sustained signaling, follows the feedback loops the axis runs on, traces the IGF-1 rise over weeks, and looks at what the trials observed happening to visceral fat.

Key terms

Pulsatile signal versus sustained elevation


The feedback loops that self-limit


From GH pulses to a steadier IGF-1


How IGF-1 shrinks visceral fat


What feedback limits, and what it does not