A few notes about some of the medications, as they come up in the media or medical literature:
(1) Avandia (the trade name for the medication rosiglitazone)
Note: there are already strong restrictions on the use of Avandia in Canada, related to other adverse effects of this medication that have come to light over the past years. This study is worth mentioning here because (1) PPAR-gamma signalling can be increased or decreased by various means and (2) it is an illustration of how medication can have multiple effects and un-intended consequences that may initially go un-noticed and un-suspected.
It is known that the diabetes medication rosiglitazone “increases food intake and body/fat mass as side-effects”. Rosiglitazone acts by the PPAR-gamma signalling pathway. This study was done to understand more.
- The important point is just that this medication tends (the effect will be more and less in different individuals) to increase eating and promote gains in body weight.
- Since this study suggests that the PPAR-gamma signalling may be involved in this, it is possible that any other medications or intervention that increase PPAR-gamma signalling may also promote appetite and promote weight gain.
- Note that this was an animal study plus the method of medication administration was nothing like taking oral pills
This report about the study is easier to comprehend than the abstract (linked below):
“Study finds why drug for type II diabetes makes people fat” in Medical News Today, March 2015, LINK
“ “People taking these TZDs are hungrier, and they do gain more weight. This may be a reason why,” Garretson said. “When they’re taking these drugs, it’s activating these receptors, which we believe are controlling feeding through this mechanism that we found. We discovered that activating these receptors makes our rodent animal model eat more and store more food for later, while blocking these receptors makes them eat less and store less food for later, even after they’ve been food deprived and they’re at their hungriest.” “
J Neurosci. 2015 Mar 18;35(11):4571-81. doi: 10.1523/JNEUROSCI.2129-14.2015.
“Peroxisome proliferator-activated receptor γ controls ingestive behavior, agouti-related protein, and neuropeptide Y mRNA in the arcuate hypothalamus.”
Garretson JT1, Teubner BJ2 et. al. LINK to Abstract
- “Peroxisome proliferator-activated receptor γ (PPARγ) is clinically targeted for type II diabetes treatment; however, rosiglitazone (ROSI), a PPARγ agonist, increases food intake and body/fat mass as side-effects.” (PPAR-gamma)
- “Thus, we demonstrated that PPARγ activation is sufficient to trigger food hoarding/intake, increase AgRP/NPY, and possibly is necessary for FD-induced increases in feeding and AgRP/NPY. These findings provide initial evidence that FD-induced increases in AgRP/NPY may be a direct PPARγ-dependent process that controls ingestive behaviors.” (FD = Food Deprivation)