12 January - 20 June 2016

Mice with reduced sense of smell resistant to diet-induced obesity, study finds

A study conducted by researchers from various institutions in the US and Germany, published in Cell Metabolism, suggests that sense of smell can affect metabolic health and obesity and specifically that mice with a reduced sense of smell are “resistant to diet-induced obesity”.

A study conducted by researchers from various institutions in the US and Germany, published in Cell Metabolism, suggests that sense of smell can affect metabolic health and obesity and specifically that mice with a reduced sense of smell are “resistant to diet-induced obesity”.

Riera et al. note that the regulation of body energy balance relies on an ”intricate balance between food intake and energy expenditure” and indicate that they consider the sense of smell is likely to contribute to the regulation of this balance.  They cite previous studies which have indicated that “sensory perception of a hidden food cue without its ingestion” can alter neuron activity and suggest that olfactory signals might allow the brain to “adapt systemic metabolism under conditions of anticipated food intake”.

To investigate this, Riera et al. induced temporary deficiency in the sense of smell in 7-week old mice and observed body weight when mice were fed normal chow or a high-fat diet (HFD) and discovered that on the HFD, the mice with the diminished sense of smell showed a 16% reduction in body weight compared to the controls also fed a HFD.  Although the smell-deficient mice fed a HFD did reduce their food intake, the researchers note that their ability to feed after overnight fasting was not reduced and so they conclude that “the lack of olfactory input leads to a lean phenotype that is not due to a loss of appetite”. Riera et al. next temporarily removed the sense of smell, by injection, in glucose-intolerant mice that were already obese due to increased calorie intake.  They discovered that a single injection reduced adiposity while repeated injections over a period of time maintained a reduced body weight and fat mass even when these mice were still fed a HFD and food intake was not reduced. The study notes that this was “mediated by increase energy expenditure”. Finally, Riera et al. wanted to examine if an increased sense of smell would worsen metabolic health. Mice genetically altered to increase olfactory stimulation were fed normal chow and the researchers found these mice showed a significant age-related weight gain and excessive adipose tissue mass in certain areas when compared to control mice.

In discussion, Riera et al suggest that the reduced olfactory inputs of the smell-deficient mice prolonged sympathetic nervous system responses and increased their fat burning capability by turning beige fat cells in to brown fat cells.  They note that in humans, loss of smell is often accompanied by loss of flavour and “subsequent loss of appetite and weight loss” but indicate that the current study showed a fatty mass decrease in mice without “overt food aversion”. Riera et al state that their study shows therefore that “reduced olfactory output triggers a metabolic response mimicking the cessation of feeding” which in turn protects animals from a high-calorie diet.

Celine Riera is quoted in a press release as saying that “People with eating disorders sometimes have a hard time controlling how much food they are eating and they have a lot of cravings. We think olfactory neurons are very important for controlling pleasure of food and if we have a way to modulate this pathway, we might be able to block cravings in these people and help them with managing their food intake”. The study concludes by saying that their data “shows that even a relatively short-term loss of smell improved metabolic health and weight loss, despite the negative consequences of being on a HFD”

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