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Glucose and Lipid Homeostasis and Inflammation in Humans Following an Isocaloric Ketogenic Diet.
Obesity (Silver Spring). 2019 Jun; 27(6):971-981.O

Abstract

OBJECTIVE

The objective of this study was to measure changes in glucose, lipid, and inflammation parameters after transitioning from a baseline diet (BD) to an isocaloric ketogenic diet (KD).

METHODS

Glucose homeostasis, lipid homeostasis, and inflammation were studied in 17 men (BMI: 25-35 kg/m2) during 4 weeks of a BD (15% protein, 50% carbohydrate, 35% fat) followed by 4 weeks of an isocaloric KD (15% protein, 5% carbohydrate, 80% fat). Postprandial responses were assessed following mixed-meal tests matched to compositions of the BD (control meal [CM]) and KD (ketogenic meal).

RESULTS

Fasting ketones, glycerol, free fatty acids, glucagon, adiponectin, gastric inhibitory peptide, total and low-density lipoprotein cholesterol, and C-reactive protein were significantly increased on the KD. Fasting insulin, C-peptides, triglycerides, and fibroblast growth factor 21 were significantly decreased. During the KD, the glucose area under the curve was significantly higher with both test meals, and the insulin area under the curve was significantly higher only for the CM. Analyses of glucose homeostasis suggested that the KD insulin sensitivity decreased during the CM but increased during the ketogenic meal. Insulin-mediated antilipolysis was decreased on the KD regardless of meal type.

CONCLUSIONS

Switching to the KD was associated with increased cholesterol and inflammatory markers, decreased triglycerides, and decreased insulin-mediated antilipolysis. Glucose homeostasis parameters were diet dependent and test meal dependent.

Links

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Authors+Show Affiliations

Rosenbaum M
Departments of Pediatrics and Medicine, Division of Molecular Genetics, Columbia University Irving Medical Center, New York, New York, USA.
Hall KD
National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Guo J
National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Ravussin E
Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA.
Mayer LS
Department of Psychiatry, New York State Psychiatric Institute, Columbia University Irving Medical Center, New York, New York, USA.
Reitman ML
National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Smith SR
The Translational Research Institute for Metabolism and Diabetes, Orlando, Florida, USA.
Walsh BT
Department of Psychiatry, New York State Psychiatric Institute, Columbia University Irving Medical Center, New York, New York, USA.
Leibel RL
Departments of Pediatrics and Medicine, Division of Molecular Genetics, Columbia University Irving Medical Center, New York, New York, USA.

MeSH

AdultBlood GlucoseDiet, KetogenicHomeostasisHumansInflammationLipidsMale

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural

Language

eng

PubMed ID

31067015

Clinical Trial Links

Clinical trial which this article describes

Citation

Rosenbaum, Michael, et al. "Glucose and Lipid Homeostasis and Inflammation in Humans Following an Isocaloric Ketogenic Diet." Obesity (Silver Spring, Md.), vol. 27, no. 6, 2019, pp. 971-981.
Rosenbaum M, Hall KD, Guo J, et al. Glucose and Lipid Homeostasis and Inflammation in Humans Following an Isocaloric Ketogenic Diet. Obesity (Silver Spring). 2019;27(6):971-981.
Rosenbaum, M., Hall, K. D., Guo, J., Ravussin, E., Mayer, L. S., Reitman, M. L., Smith, S. R., Walsh, B. T., & Leibel, R. L. (2019). Glucose and Lipid Homeostasis and Inflammation in Humans Following an Isocaloric Ketogenic Diet. Obesity (Silver Spring, Md.), 27(6), 971-981. https://doi.org/10.1002/oby.22468
Rosenbaum M, et al. Glucose and Lipid Homeostasis and Inflammation in Humans Following an Isocaloric Ketogenic Diet. Obesity (Silver Spring). 2019;27(6):971-981. PubMed PMID: 31067015.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glucose and Lipid Homeostasis and Inflammation in Humans Following an Isocaloric Ketogenic Diet. AU - Rosenbaum,Michael, AU - Hall,Kevin D, AU - Guo,Juen, AU - Ravussin,Eric, AU - Mayer,Laurel S, AU - Reitman,Marc L, AU - Smith,Steven R, AU - Walsh,B Timothy, AU - Leibel,Rudolph L, Y1 - 2019/05/08/ PY - 2018/12/12/received PY - 2019/02/22/accepted PY - 2019/5/9/pubmed PY - 2020/3/12/medline PY - 2019/5/9/entrez SP - 971 EP - 981 JF - Obesity (Silver Spring, Md.) JO - Obesity (Silver Spring) VL - 27 IS - 6 N2 - OBJECTIVE: The objective of this study was to measure changes in glucose, lipid, and inflammation parameters after transitioning from a baseline diet (BD) to an isocaloric ketogenic diet (KD). METHODS: Glucose homeostasis, lipid homeostasis, and inflammation were studied in 17 men (BMI: 25-35 kg/m2) during 4 weeks of a BD (15% protein, 50% carbohydrate, 35% fat) followed by 4 weeks of an isocaloric KD (15% protein, 5% carbohydrate, 80% fat). Postprandial responses were assessed following mixed-meal tests matched to compositions of the BD (control meal [CM]) and KD (ketogenic meal). RESULTS: Fasting ketones, glycerol, free fatty acids, glucagon, adiponectin, gastric inhibitory peptide, total and low-density lipoprotein cholesterol, and C-reactive protein were significantly increased on the KD. Fasting insulin, C-peptides, triglycerides, and fibroblast growth factor 21 were significantly decreased. During the KD, the glucose area under the curve was significantly higher with both test meals, and the insulin area under the curve was significantly higher only for the CM. Analyses of glucose homeostasis suggested that the KD insulin sensitivity decreased during the CM but increased during the ketogenic meal. Insulin-mediated antilipolysis was decreased on the KD regardless of meal type. CONCLUSIONS: Switching to the KD was associated with increased cholesterol and inflammatory markers, decreased triglycerides, and decreased insulin-mediated antilipolysis. Glucose homeostasis parameters were diet dependent and test meal dependent. SN - 1930-739X UR - https://www.unboundmedicine.com/medline/citation/31067015/full_citation DB - PRIME DP - Unbound Medicine ER -
Grapherence [↓69 ↑42]

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