Dietary sugar consumption has dramatically risen in the U.S. over the past 60 years 1. In addition to being associated with body weight gain and harmful metabolic outcomes 2-7, emerging evidence reveals that excessive consumption of sugar and other ?obesogenic? dietary factors (e.g., saturated fatty acids) negatively impacts memory function and other cognitive processes 8,9. Particularly concerning is the rise in sugar consumption among children, who with ~15-20% of their total daily caloric intake from added sugars (predominantly from sugar-sweetened beverages, SSBs) 10,11, are the highest sugar consumers of any age group. The juvenile and adolescent developmental phases are highly susceptible periods for the onset of metabolic dysfunction resulting from excessive sugar intake 6 and new evidence suggests that this period of development is also a particularly vulnerable time for sugar-related neurocognitive deficits 12,13. Therefore, it is important to understand the precise developmental periods and domains of cognition that are vulnerable to excessive consumption of added sugars during early life periods. Our preliminary data presented herein reveals that excessive consumption of SSBs (11% carbohydrate solution to match commonly consumed SSBs in the U.S.) in rats beginning at the onset of the juvenile period of development but not beginning during early adulthood impairs spatial memory function and increases neuroinflammation in the hippocampus 14, a brain region classically associated with spatial and declarative memory function and more recently with learned aspects of food intake control 15,16. Other preliminary data presented in this proposal offer insight into possible mechanisms linking early life sugar consumption with hippocampal-dependent memory impairments, as early life SSB access profoundly alters the gut microbiome and reduces markers of neurogenesis in the hippocampus. Proposed experiments will provide mechanistic insight into the relationship between early life sugar consumption and memory impairment by illuminating [1] the precise developmental periods and feeding- relevant memory processes that are particularly vulnerable to early life sugar consumption, [2] the underlying neurobiological mechanisms through which dietary factors during development influence cognition, and [3] intervention strategies that can potentially reverse the long-lasting memory deficits associated with excessive early life sugar consumption. Results will contribute toward understanding the underlying mechanisms through which obesogenic dietary factors influence cognition and may provide valuable insight toward reversing or preventing the pathological effects of unhealthy dietary factors on the brain.

Public Health Relevance

An important factor contributing to the obesity epidemic in the United States is the exponential rise in the consumption of added sugars. In addition to being associated with body weight gain and negative metabolic outcomes, sugar consumption, particularly during early life periods of development, is associated with cognitive impairment. Here we investigate the mechanisms through which early life consumption of sugars negatively affects memory function and feeding-related behaviors later in life.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project (R01)
Project #
5R01DK123423-02
Application #
10020400
Study Section
Biobehavioral Regulation, Learning and Ethology Study Section (BRLE)
Program Officer
Cooke, Brad
Project Start
2019-09-20
Project End
2023-07-31
Budget Start
2020-08-01
Budget End
2021-07-31
Support Year
2
Fiscal Year
2020
Total Cost
Indirect Cost
Name
University of Southern California
Department
Biology
Type
Schools of Arts and Sciences
DUNS #
072933393
City
Los Angeles
State
CA
Country
United States
Zip Code
90089