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Obesity (Silver Spring). 2018 Sep;26(9):1448-1456. doi: 10.1002/oby.22263.

Effects of Chronic NAD Supplementation on Energy Metabolism and Diurnal Rhythm in Obese Mice.

Author information

1
Appetite Regulation Laboratory, Asan Institute for Life Sciences, Seoul, Korea.
2
Department of Translational Medicine, University of Ulsan College of Medicine, Seoul, Korea.
3
Department of Biomedical Science, University of Ulsan College of Medicine, Seoul, Korea.
4
Department of Biomedical Science, Korea University College of Medicine, Seoul, Korea.
5
Division of Endocrinology and Metabolism, Asan Medical Center, Seoul, Korea.

Abstract

OBJECTIVE:

Adequate nicotinamide adenine dinucleotide (NAD) content in hypothalamic neurons is critical for the maintenance of normal energy balance and circadian rhythm. In this study, the beneficial metabolic effects of chronic NAD supplementation on diet-induced obesity and obesity-related disruption of diurnal rhythms were examined.

METHODS:

C57BL/6 mice were fed a high-fat diet (HFD) for 12 weeks and received an intraperitoneal injection of either saline or NAD (1 mg/kg/day) for the last 4 weeks. The control mice were fed a chow diet and injected with saline for the same period. Body weights were monitored daily. Daily rhythms of food intake, energy expenditure, and locomotor activity were measured at the end of NAD treatment. The effect of NAD treatment on the clock gene Period 1 (PER1) transcription was also studied.

RESULTS:

Chronic NAD supplementation significantly attenuated weight gain in HFD-fed obese mice. Furthermore, NAD treatment recovered the suppressed rhythms in the diurnal locomotor activity patterns in obese mice. In addition, exogenous NAD supply rescued cellular NAD depletion-induced suppression of PER1 transcriptional activity in hypothalamic neuron cells as well as blunted daily fluctuations of hypothalamic arcuate nucleus PER1 expression in obese mice.

CONCLUSIONS:

NAD supplementation showed therapeutic effects in obese mice with altered diurnal behaviors.

PMID:
30230244
DOI:
10.1002/oby.22263

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