Obesity is a problem of epidemic proportions that causes many serious health related complications. This week, MedZine emphasizes two studies on different aspects of appetite, which controls dietary intake and thus is important for obesity. These studies describe changes in the tongue of obese individuals and a process that influences hormone levels that induce appetite.
Impaired detection of sweetness
The taste system is one of the neuronal systems that regulate appetite; still no one had ever looked at the cells on the tongue that make contact with food. Maliphol and colleagues now describe in a publication in PLoS ONE that obese mice have fewer taste cells that responded to sweet stimuli than slim mice. In addition, the taste cells that are present don’t respond as well as the cells in normal mice. This was investigated by measuring calcium signaling in taste cells and followed up with behavioral studies. According to the researchers, it’s possible that problems in detecting sweetness may encourage obese mice to eat more than their leaner counterparts to get the same payoff.
Ghrelin is bound by immunoglobulins that modify its stability
Ghrelin is the main orexigenic, meaning appetite stimulating, hormone. Despite normal plasma levels of ghrelin, obese individuals often have increased appetite. Research by Takagi and colleagues, published in Nature Communications, shows that immunoglobulins bind ghrelin in obese individuals and prevent its degradation. The study shows that the IgG-immunoglobulins display increased binding affinity for ghrelin in obese humans and mice. This enhanced binding increases ability of this IgG to transport ghrelin and thus enhance its orexigenic actions. Administering IgG extracted from plasma of obese humans or mice enhances food intake, meal frequency and total body mass in mice. The researchers therefore suggest that ghrelin-reactive immunoglobulins increases appetite and overeating in obesity.
Sources: PLoS ONE, University of Buffalo, and Nature Communications