Now, Tagaki and colleagues from Rouen University, France, in a paper published in Nature Communications, suggests that some people may have more pronounced and extended hunger due to to ghrelin-stabilizing immunoglobulins (IgG).
In their experiments in mice showed that ghrelin degradation is inhibited by certain anti-ghrelin IgG with increased binding affinity foundnin the plasma of obese but not of anorectic or non-obese individuals.
They also showed that repeated injections of ghrelin together with IgG from ob/ob mice resulted in increase food intake, meal frequency and total lean body mass of normal mice.
These findings suggest that ghrelin-specific IgG may play a role in modulating hunger and food intake in obese humans and animals.
This would not be the first example of such interactions between auto-antibodies and hormones, but does point to a new passible pathway to explain why some people, despite having “normal” ghrelin levels may experience more hunger than others.
While these findings may not lead directly to a better treatment for obesity, they do remind us of the complexity of hunger and the physiology of ingestive behaviour.
I guess, when you are hungry, pushing away from the table is simply not an option.
Takagi K, Legrand R, Asakawa A, Amitani H, François M, Tennoune N, Coëffier M, Claeyssens S, do Rego JC, Déchelotte P, Inui A, & Fetissov SO (2013). Anti-ghrelin immunoglobulins modulate ghrelin stability and its orexigenic effect in obese mice and humans. Nature communications, 4 PMID: 24158035