The growing prevalence of obesity in western societies represents a critical public health concern to millions of people, yet the factors controlling the buildup of fat within our bodies are not completely understood.
The involuntary functions of organs such as the heart, stomach and intestines are regulated by the autonomic nervous system. This system is divided into two parts – the sympathetic nervous system (SNS) and parasympathetic nervous system (PSNS). The SNS controls our body’s reactions during “fight or flight” situations where heart rate, blood pressure, and energy usage are increased. The primary source of stored energy in mammals are fat deposits and if energy needs cannot be met during “fight or flight” situations, signals sent from the brain via the SNS to fat cells – a process known as SNS innervation – induces the breakdown of fat and the release of extra fuel.
On the other hand, the PSNS controls our body during “rest and digest” situations where the body is relaxed and digestion is increased. While it has been demonstrated that dual SNS and PSNS innervation exists in most organs, no such innervation by the PSNS has been demonstrated for fat cells. If present, PSNS innervation may begin to explain the complex mechanisms underlying the buildup of fatty tissue.
A study reported in the November 4 issue of the Journal of Clinical Investigation (JCI) by Felix Kreier and colleagues from the Netherlands Institute for Brain Research in Amsterdam revealed, for the first time, that PSNS innervation of fatty tissue does indeed occur.
The authors removed nerves from the sympathetic branch of the nervous system of rats and injected multiple abdominal fat compartments with molecular tagged pseudorabies virus. The replication of viral particles resulted in infections occurring only along the chain of functionally–connected neurons of the PSNS from the fatty tissue to the brain.
“Before this work, there was little or no evidence for the PSNS innervation of white adipose tissue” noted Timothy Bartness from the Department of Biology and Center for Behavioral Neuroscience at Georgia State University, Atlanta, in his accompanying Commentary in the JCI.
The authors also demonstrated that individual neurons are specialized to control one fat compartment. Dr. Bartness writes further “this could result in enhanced regional accumulation of lipid with certain pathologies. This expansion of the adipose organ in these areas could lead to several well-known adverse health consequences of enhanced visceral/abdominal adiposity such as type II diabetes, certain cancers and high blood pressure.” However more work is necessary to reveal whether the nerves described participate in naturally-occurring lipid accumulation, or alternatively are associated with disease-related obesity states.