Format

Send to

Choose Destination
See comment in PubMed Commons below
Am J Physiol Regul Integr Comp Physiol. 2017 Jul 12:ajpregu.00067.2017. doi: 10.1152/ajpregu.00067.2017. [Epub ahead of print]

Low carbohydrate diet induces metabolic depression: a possible mechanism to conserve glycogen.

Author information

1
University of Queensland h.winwoodsmith@uq.edu.au.
2
University of Queensland.

Abstract

Long-term studies have found low carbohydrate diets are more effective for weight loss than calorie restricted diets in the short-term, but equally or only marginally more effective in the long-term. Low carbohydrate diets have been linked to reduced glycogen stores and increased feelings of fatigue. We propose that reduced physical activity in response to lowered glycogen explains the diminishing weight loss advantage of low carbohydrate compared to low calorie diets over longer time scales. We explored this possibility by feeding adult Drosophila melanogaster either a standard or low carbohydrate diet for nine days and measured changes in metabolic rate, glycogen stores, activity, and body mass. We hypothesized that a low carbohydrate diet would cause a reduction in glycogen stores that recovers over time, reduced physical activity, and an increase in resting metabolic rate. The low carbohydrate diet was found to reduce glycogen stores, which recovered over time. Activity was unaffected by diet but the low carbohydrate group experienced a reduction in metabolic rate. We conclude that metabolic depression could explain the decreased effectiveness of low carbohydrate diets over time and recommend further investigation of long-term metabolic effects of dietary interventions and a greater focus on physiological plasticity within the study of human nutrition.

KEYWORDS:

drosophila; nutrition; obesity; plasticity; protein

PMID:
28701319
DOI:
10.1152/ajpregu.00067.2017
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Support Center