Study Spotlight Take-Away with Chef Dr. Mike: The See Food Diet

by Michael S. Fenster, MD

“To me, food is as much about the moment, the occasion, the location, and the company as it is about the taste.”

Heston Blumenthal, Three Michelin Starred Chef
 

Scientists generally regard the beginning of digestion as the moment we begin the mechanical action of chewing to break food into smaller pieces. Many chefs believe the act of eating begins when we see and smell the food. According to a recent paper published by researchers at the esteemed Max Planck Institute for Metabolism Research in Cologne, Germany, it appears that chefs may have been right all along.

What chefs refer to is known as the cephalic phase of gustation. This is the phase of experience that occurs before food enters the stomach. It is triggered by the sight, smell, taste, or even the thought of food. When this happens, certain neural pathways are activated, often involving the vagus nerve as part of the Gut-Brain Axis. The digestive system, including the stomach, intestines, pancreas, and liver, begins to rev up the cellular machinery necessary to process the anticipated meal. The current research shows that in mice these adaptations occur in the liver mitochondria after only a few minutes of being exposed to the sight and smell of food. These particular changes in the liver mitochondria play a role in the body’s metabolism of sugar and could have important ramifications for the diagnosis and treatment of type 2 diabetes.

The Study:

  • The study utilized a murine model in which the mice were subject to a 16-hour fast.
  • The mice were broken into three groups:
    • Those who had their liver profile examined after fasting;
    • Those who had the liver profile examined after fasting and being exposed to the smell and sight of food but were not allowed to access the food and eat;
    • Those who had their liver profile examined after fasting and being exposed to the smell and sight of food but were allowed to eat.
  • The effects were measured by looking at specific changes in mitochondrial architecture.
  • These specific changes are associated with how the body handles insulin sensitivity, which is impaired in type II diabetes and a hallmark of the disease.
  • The study showed that sensory exposure, such as smell and sight of food, but not necessarily actual food consumption, was sufficient to cause changes in the mitochondria of liver cells within minutes.

Caveat:

This study examined the effects of seeing and smelling food but not necessarily eating it on mitochondria located in liver cells. Mitochondria are dynamic organelles that play a key role in energy conversion. In response to certain stimuli, mitochondria undergo structural changes such as fission or fusion, which involves changes to the organelle’s outer and inner membranes. Unopposed fission causes mitochondrial fragmentation, which is generally associated with metabolic dysfunction and diseases such as obesity, insulin resistance, and type II diabetes.[1] Unopposed fusion results in a hyperfused network and serves to “counteract metabolic insults, preserve cellular integrity, and protect against autophagy.”[2] Optimal mitochondrial function is ensured by a quality-control system tightly coupled to fusion and fission.[3]

In this study, the researchers analyzed the mitochondria in the livers of mice and found that processes normally stimulated by food intake were activated within minutes by only the sight and smell of food. The changes undergone by the mitochondria affect the sensitivity of the liver to insulin. This newly discovered signaling pathway helps regulate insulin sensitivity within the body and has implications for the diagnosis and treatment of type II diabetes, in which insulin sensitivity is impaired.

This research demonstrates that simply the sensory perception of food without actual consumption is enough to initiate a cascade of biological processes throughout the body, including hepatic effects involving glucose metabolism. These effects do not occur hours after we start eating and require us to begin to digest our food but within minutes of the sensory anticipation of the meal. As it applies to the food experience, seeing is believing – or at least, in this case, digesting.


[1] (Hammerschmidt, 2019)

[2] (Wai, 2016)

[3] (Sebastián, 2012)


The Study:

Henschke, S.; Nolte, H.; Magoley, J.; Kleele, T.; Brandt, C.; Hausen, AC.; Wunderlich, CM.; Bauder, CA.; Aschauer, P.; Manlwy, S.; Langer, T.; Wunderlich, FT.; Bruning, JC. Food perception promotes phosphorylation of MFFS131 and mitochondrial fragmentation in liver. Science. 2024; 384, 438-446. DOI:10.1126/science.adk1005.


Additional resources:

Hammerschmidt P, Ostkotte D, Nolte H, Gerl MJ, Jais A, Brunner HL, Sprenger HG, Awazawa M, Nicholls HT, Turpin-Nolan SM, Langer T, Krüger M, Brügger B, Brüning JC. CerS6-Derived Sphingolipids Interact with Mff and Promote Mitochondrial Fragmentation in Obesity. Cell. 2019; 177(6):1536-1552.e23. doi:10.1016/j.cell.2019.05.008.

Lin HY, Weng SW, Chang YH, Su YJ, Chang CM, Tsai CJ, Shen FC, Chuang JH, Lin TK, Liou CW, Lin CY, Wang PW. The Causal Role of Mitochondrial Dynamics in Regulating Insulin Resistance in Diabetes: Link through Mitochondrial Reactive Oxygen Species. Oxid Med Cell Longev. 2018 Sep 30;2018:7514383. doi: 10.1155/2018/7514383.

Power ML, Schulkin J. Anticipatory physiological regulation in feeding biology: cephalic phase responses. Appetite. 2008; 50(2-3):194-206. doi:10.1016/j.appet.2007.10.006.

Sebastián D, Hernández-Alvarez MI, Segalés J, Sorianello E, Muñoz JP, Sala D, Waget A, Liesa M, Paz JC, Gopalacharyulu P, Orešič M, Pich S, Burcelin R, Palacín M, Zorzano A. Mitofusin 2 (Mfn2) links mitochondrial and endoplasmic reticulum function with insulin signaling and is essential for normal glucose homeostasis. Proc Natl Acad Sci U S A. 2012; 109(14):5523-8. doi: 10.1073/pnas.1108220109.

Wai T, Langer T. Mitochondrial Dynamics and Metabolic Regulation. Trends Endocrinol Metab. 2016; 27(2):105-117. doi:10.1016/j.tem.2015.12.001

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