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Type 2 diabetes: A side effect of the adaptation of neurons and fat cells to support increased cognitive performance

Lookup NU author(s): Dr Peter Andras, Dr Alina Andras

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Abstract

Type 2 diabetes is a serious disease that is affecting an increasing part of the population in most countries. A new hypothesis is presented in this paper about the underlying causes and mechanisms that lead to the development of this disease. It is proposed that the disease is the price that the organism pays for having improved cognitive performance that is achieved through increased level of neurite growth dynamics of neurons. The suggested mechanism of the disease development involves neural centres that deal with the sensing of fat and sugar levels in the blood and cerebro-spinal fluid, the regulation of the mobilisation of these resources in the body, the regulation of the storage of sugar and fat in the body, and the regulation of feeding behaviour. The key idea of the proposed mechanism is that the hypothesised resource mobilisation neural centre overestimates the resource needs of neurons and generates and inflated resource requesting signals. The paper discusses how short- and long-term equilibrium regulation of fat and sugar resources may emerge and how this regulation may get imbalanced leading to the emergence of type 2 diabetes in the animal or human. The paper proposes a number of experimental tests that can confirm or deny the validity of the hypothesis formulated here. Possible implications for development of new drugs aimed to prevent or reduce the negative impacts of type 2 diabetes are also discussed. (C) 2012 Elsevier Ltd. All rights reserved.

Publication metadata

Author(s): Andras P, Andras A

Publication type: Article

Publication status: Published

Journal: Medical Hypotheses

Year: 2013

Volume: 80

Issue: 2

Pages: 176-185

Print publication date: 01/02/2013

ISSN (print): 0306-9877

ISSN (electronic): 1532-2777

Publisher: Churchill Livingstone

URL: http://dx.doi.org/10.1016/j.mehy.2012.11.023

DOI: 10.1016/j.mehy.2012.11.023

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