Diet-Induced Changes in AChE Activity after Long-Term Exposure Rosilene R. Kaizer, 1 Adriane C. da Silva, 1 Vera M. Morsch, 1 Maisa C. Correˆa, 1 and Maria R. C. Schetinger 1, 2 (Accepted July 6, 2004) In the present study we investigated a potential mechanism by which high sugar (HS) and high fat (HF) diets could affect acetylcholinesterase (AChE) activity. The treatment with HS and HF diet was done for six months on male and female rats. The results showed decreased hippocampal AChE activity in male and females receiving HS and HF diets (HS 24% and 36%; HF 38% and 32%, males and females, respectively; P < 0.05). The activity in the cerebral cortex was reduced in males (49 and 40%) and females (19 and 17%) (P < 0.05) on HS and HF diets, respectively. In the hypothalamus AChE activity was decreased on HS diet in males (46%) and female (25%) (P < 0.05) and also on HF diet in males (34%) and females (21%) (P < 0.05). However, in the cerebellum no changes in AChE activity were observed. These results indicate that HS and HF diets produced mainly inhibition in acetylcholine degradation. It probably indicates a chronic alteration induced by these diets on the cholinergic system. KEY WORDS: AChE, Acetylcholine, diets, high sugar, high fat. INTRODUCTION It is currently well accepted that lifestyle plays a critical role in maintaining neural function in the life course of individuals. Studies mainly focus on diets typical of most industrialized Western societies, rich in saturated fat and refined sugar (HFS) (1). The possibility that high sugar (HS) and high fat (HF) diets affect neural function would indicate that diet can increase vulnerability to numerous neu- rological diseases. Thus, it is important to determine the influence of dietary factors in modifying specific aspects of neuronal health and function (2). Acetylcholine (ACh) is a neurotransmitter of pivotal importance in CNS function and is related to learning, memory, cortical organization of move- ment, and the control of cerebral blood flow (3). This neurotransmitter is synthesized in the nerve endings of the presynaptic nerve from choline and acetyl coenzyme A (acetyl CoA). Acetyl CoA is a product of cell metabolism, and choline is derived from lipid metabolism. After release, acetylcholine is hydro- lyzed to choline and acetate by acetylcholinesterase (EC 3.1.1.7; AChE), and other non-specific esterases (4). AChE is an important regulatory enzyme that controls the transmission of nerve impulses across cholinergic synapses (5) and its activity is considered a good indicator of cholinergic activity (3). Cholinesterases such as AChE and BuChE (bu- tyrylcholinesterase) participate in the hydrolysis and 1 Departamento de Quı´mica, Centro de Cieˆncias Naturais e Exa- tas, Universidade Federal de Santa Maria, Av. Roraima, Cep 97119-900, Santa Maria, RS, Brazil. 2 Address reprint requests to: Maria Rosa Chitolina Schetinger, Fax: +55-55-2208978; Depto. de Quı´mica , CCNE, Universid- ade Federal de Santa Maria, Av. Roraima, 97105-900, Santa Maria, RS, Brazil. E-mail: mariarosa@smail.ufsm.br 2251 0364-3190/04/1200–2251/0 Ó 2004 Springer Science+Business Media, Inc. Neurochemical Research, Vol. 29, No. 12, December 2004 (Ó 2004), pp. 2251–2255