STUDY SHOWS THAT EVERY MEAL TRIGGERS INFLAMMATION


Every meal triggers inflammation
January 16, 2017
Universität Basel
When we eat, we do not just take in
nutrients – we also consume a
significant quantity of bacteria. The body
is faced with the challenge of
simultaneously distributing the ingested
glucose and fighting these bacteria. This
triggers an inflammatory response that
activates the immune systems of healthy
individuals and has a protective effect,
as doctors have proven for the first time.
In overweight individuals, however, this
inflammatory response fails so
dramatically that it can lead to diabetes.
Cite This Page :
Universität Basel. "Every meal triggers inflammation."
ScienceDaily. ScienceDaily, 16 January 2017.
<www.sciencedaily.com/
releases/2017/01/170116121912.htm>.
FULL STORY
When we eat, we do not just take in nutrients --
we also consume a significant quantity of
bacteria. The body is faced with the challenge of
simultaneously distributing the ingested glucose
and fighting these bacteria. This triggers an
inflammatory response that activates the immune
systems of healthy individuals and has a
protective effect, as doctors from the University
and the University Hospital Basel have proven for
the first time. In overweight individuals, however,
this inflammatory response fails so dramatically
that it can lead to diabetes.
It is well known that type 2 diabetes (or adult-onset
diabetes) leads to chronic inflammation with a range of
negative impacts. A number of clinical studies have
therefore treated diabetes by impeding the over-
production of a substance involved in this process,
Interleukin-1beta (IL-1beta). In diabetes patients, this
messenger substance triggers chronic inflammation and
causes insulin-producing beta cells to die off.
Activation of the immune system
This inflammation does have some positive aspects,
however, as was recently reported in the journal Nature
Immunology by researchers from the Department of
Biomedicine at the University and the University Hospital
Basel. In healthy individuals, short-term inflammatory
responses play an important role in sugar uptake and the
activation of the immune system.
In their work, Professor Marc Donath, Head of the
Department of Endocrinology, Diabetes and Metabolism at
the University Hospital Basel and his research team
demonstrate that the number of macrophages (a type of
immune cell) around the intestines increases during meal
times. These so-called "scavenger cells" produce the
messenger substance IL-1beta in varying amounts,
depending on the concentration of glucose in the blood.
This, in turn, stimulates insulin production in pancreatic
beta cells. The insulin then causes the macrophages to
increase IL-1beta production. Insulin and IL-1beta work
together to regulate blood sugar levels, while the
messenger substance IL-1beta ensures that the immune
system is supplied with glucose and thus remains active.
Bacteria and nutrients
According to the researchers, this mechanism of the
metabolism and immune system is dependent on the
bacteria and nutrients that are ingested during meals.
With sufficient nutrients, the immune system is able to
adequately combat foreign bacteria. Conversely, when
there is a lack of nutrients, the few remaining calories
must be conserved for important life functions at the
expense of an immune response. This may go some way
towards explaining why infectious diseases occur more
frequently in times of famine.
Story Source:
Materials provided by Universität Basel . Note: Content
may be edited for style and length.
Journal Reference :
1. Erez Dror, Elise Dalmas, Daniel T Meier, Stephan
Wueest, Julien Thévenet, Constanze Thienel,
Katharina Timper, Thierry M Nordmann, Shuyang
Traub, Friederike Schulze, Flurin Item, David Vallois,
Francois Pattou, Julie Kerr-Conte, Vanessa
Lavallard, Thierry Berney, Bernard Thorens, Daniel
Konrad, Marianne Böni-Schnetzler & Marc Y Donath.
Postprandial macrophage-derived IL-1β stimulates
insulin and both synergistically promote glucose
disposal and inflammation . Nature Immunology ,
January 2017 DOI: 10.1038/ni.3659

Comments

Popular Posts