CRU 126, Subproject: Selfish Brain - Brain Glucose and Metabolic Syndrome

Project: DFG ProjectsDFG Joint Research: Research Units/ Clinical Research Units

Project Details


The exact regulation of brain glucose level in higher organisms is crucial to their survival. A lack of brain glucose can not only generate cognitive dysfunction, very low blood glucose levels can cause convulsions, loss of consciousness, and in the worst case even lead to death. There is a traditional paradigm concerning blood glucose regulation. The 14th edition of Harrison s Principals of internal medicine states, The maintenance of plasma glucose concentrations within narrow bounds is essential for health. Here, we formulate a novel paradigm, by changing plasma glucose into brain glucose .
This novel and fundamental paradigm has been extensively discussed in our Review The Selfish Brain: Competition for Energy Resources (Neuroscience Biobehavioral Reviews, 2004). This basic paradigm is the link of all our projects. The main goal of the Clinical Research Unit is to prepare a change in paradigm by establishing a novel point of view.
Our theory comprises four basic principles:
-- First, the brain prioritises the adjustment of its own ATP concentration. High and low affinity ATP-sensitive potassium channels regulate the brain s self-allocation of glucose.
-- Second, brain ATP regulation is a learning control process. The self-allocation process is under short-term and long-term feedback control by cortisol and its high and low-affinity receptors.
-- Third, the brain uses cortical plasticity to stabilise the self-allocation process in the long run. After a stressful experience, a newly achieved consolidation and stabilisation of the self-allocation process may allow the brain to reappraise its energy demand strategies.
-- Fourth, alterations in glucose allocation can be compensated by changes in food intake or by utilisation of alternate substrates such as lactate or ketones. Alternative strategies of the brain to safeguard its energy needs can result in diseases like obesity and type 2 diabetes mellitus.
In contrast to conventional models our paradigm alters the hierarchy of regulated parameters by prioritising the energy demand of the brain and giving it a supreme authority. The dimension of adipose tissue as well as the dimension of muscle tissue becomes a regulating goal of second order. According to this idea obesity and type 2 diabetes are central diseases of the brain on the basis of neuroendocrine defects. Efforts to prevent and treat obesity can therefore only be successful when taking into account these crucial aspects.

Key findings

Zusammenfassend bereiten die theoretischen und experimentellen Ergebnisse der KFO 126 einen Paradigmenwechsel im Feld der Adipositasforschung vor. Früher wurde die aktive Rolle des Gehirns, welches nachgewiesenermaßen „aktiv“ Energie aus dem Körper anfordert, nicht hinreichend berücksichtigt. Dieser Gesichtspunkt ist aber für ein tiefes Verständnis des Energiestoffwechsels unabdingbar. Aus neuroenergetischer Perspektive ergibt sich durch die Arbeiten der KFO 126 ein völlig neues Bild vom menschlichen Energiestoffwechsel. Dieses hat wichtige Implikationen für die Anwendung von Maßnahmen, mit denen der Gewichtszunahme von Kindern, Jugendlichen und Erwachsenen entgegengewirkt werden kann.

Effective start/end date01.01.0531.12.10

UN Sustainable Development Goals

In 2015, UN member states agreed to 17 global Sustainable Development Goals (SDGs) to end poverty, protect the planet and ensure prosperity for all. This project contributes towards the following SDG(s):

  • SDG 3 - Good Health and Well-being

Research Areas and Centers

  • Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)

DFG Research Classification Scheme

  • 205-04 Physiology
  • 205-09 Pharmacology
  • 206-07 Clinical Neurology Neurosurgery and Neuroradiology
  • 312-01 Mathematics


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