CoChat
Sign Up
Cited by 18

The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.

The Impact of Ketogenic Nutrition on Obesity and Metabolic Health: Mechanisms and Clinical Implications

Biesiekierska, Marta, Strigini, Maura, Śliwińska, Agnieszka, Pirola, Luciano, Balcerczyk, Aneta·2025·Nutrition Reviews
DOI 10.1093/nutrit/nuaf010PMC PMC12422014
Open this paper in CoChat — free account

Abstract

The ketogenic diet (KD) has recently gained increasing popularity. This high-fat, adequate-protein, and carbohydrate-poor eating pattern leads to nutritional ketosis. The KD has long been known for its antidiabetic and antiepileptic effects and has been used therapeutically in these contexts. Recently, the KD, due to its effectiveness in inducing weight loss, has also been proposed as a possible approach to treat obesity. Likewise, a KD is currently explored as a supporting element in the treatment of obesity-associated metabolic disorders and certain forms of cancer. Here, we discuss the metabolic and biochemical mechanisms at play during the shift of metabolism to fatty acids and fatty acid–derived ketone bodies as main fuel molecules, in the substitution of carbohydrates, in ketogenic nutrition. Different sources of ketone bodies and KDs as alternatives to glucose and carbohydrates as main energy substrates are discussed, together with an attempt to weigh the benefits and risks posed by the chronic use of a KD in the context of weight loss, and also considering the molecular effects that ketone bodies exert on metabolism and on the endocrine system.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1093/nutrit/nuaf010

Cites

26 of 26 references verified0 citation errors · 0 not checkable

Statistics

Figures

Figure 1. Metabolism of Fatty Acids (FAs). (A) Ketogenesis is initiated in order to make available energy stored in fatty acids. Once formed in the mitochondria, acetyl coenzyme A (acetyl-CoA) is reversibly converted to acetoacetyl-CoA, what is catalyzed by acetyl-CoA transferase 1 (ACAT1). Next, HMG (hydroxymethylglutaryl)-CoA synthase condenses acetyl-CoA with acetoacetyl-CoA to form HMG-CoA. HMG-CoA lyase catalyzes the formation of acetoacetate from HMG-CoA. The acetoacetate (AcAc) is then reversibly converted to β-hydroxybutyrate (BHB) by β-hydroxybutyrate dehydrogenase 1 (BDH1). (B) Fatty acids are present in the blood due to prior disruption of lipids (lipolysis) and are used as substrates in the β-oxidation process. Following hepatic ketogenesis, the ketone bodies are transferred back to the blood, where BHB as a signaling metabolite can be further transferred to extrahepatic tissues and AcAc can be degraded spontaneously into acetone (Ac), which will then be exhaled. (C) Ketolysis encompasses a set of reactions designed to recover energy through the oxidation of ketone bodies, which takes place in the mitochondria. The main ketone body distributed to the extrahepatic tissues—BHB—undergoes the reversible conversion to AcAc by BDH1. AcAc is then incorporated into acetoacetyl-CoA in a reaction catalyzed by succinyl-CoA-3-ketoacid-coenzyme A transferase (SCOT). Acetoacetyl-CoA can be reversibly converted by ACAT1 to acetyl-CoA, which is used in the tricarboxylic acid (TCA) cycle. The figure was created with BioRender.com
Figure 1. Metabolism of Fatty Acids (FAs). (A) Ketogenesis is initiated in order to make available energy stored in fatty acids. Once formed in the mitochondria, acetyl coenzyme A (acetyl-CoA) is reversibly converted to acetoacetyl-CoA, what is catalyzed by acetyl-CoA transferase 1 (ACAT1). Next, HMG (hydroxymethylglutaryl)-CoA synthase condenses acetyl-CoA with acetoacetyl-CoA to form HMG-CoA. HMG-CoA lyase catalyzes the formation of acetoacetate from HMG-CoA. The acetoacetate (AcAc) is then reversibly converted to β-hydroxybutyrate (BHB) by β-hydroxybutyrate dehydrogenase 1 (BDH1). (B) Fatty acids are present in the blood due to prior disruption of lipids (lipolysis) and are used as substrates in the β-oxidation process. Following hepatic ketogenesis, the ketone bodies are transferred back to the blood, where BHB as a signaling metabolite can be further transferred to extrahepatic tissues and AcAc can be degraded spontaneously into acetone (Ac), which will then be exhaled. (C) Ketolysis encompasses a set of reactions designed to recover energy through the oxidation of ketone bodies, which takes place in the mitochondria. The main ketone body distributed to the extrahepatic tissues—BHB—undergoes the reversible conversion to AcAc by BDH1. AcAc is then incorporated into acetoacetyl-CoA in a reaction catalyzed by succinyl-CoA-3-ketoacid-coenzyme A transferase (SCOT). Acetoacetyl-CoA can be reversibly converted by ACAT1 to acetyl-CoA, which is used in the tricarboxylic acid (TCA) cycle. The figure was created with BioRender.comCC BY-NC-ND · PubMed Central
Figure 2. Changes in the Ketone Body Levels Depending on Ketone Body Sources and Metabolic Conditions. In the physiological state, concentrations of BHB are below 1 mmol/L. Overnight fasting and 24-hour fasting generate physiological ketonemia. Longer fasting, from 3 to 7 days, results in overt ketosis and the induction of ketosis through the ketogenic diet may increase the concentration of ketone bodies to up to 7 mmol/L. Starvation leads to an approximately 6–8 mmol/L blood BHB concentration, when maintained for more than 10 days. Beyond this range (up to 20 mmol/L), pathological conditions, such as untreated diabetes and ketoacidosis, occur. The figure was created with BioRender.com
Figure 2. Changes in the Ketone Body Levels Depending on Ketone Body Sources and Metabolic Conditions. In the physiological state, concentrations of BHB are below 1 mmol/L. Overnight fasting and 24-hour fasting generate physiological ketonemia. Longer fasting, from 3 to 7 days, results in overt ketosis and the induction of ketosis through the ketogenic diet may increase the concentration of ketone bodies to up to 7 mmol/L. Starvation leads to an approximately 6–8 mmol/L blood BHB concentration, when maintained for more than 10 days. Beyond this range (up to 20 mmol/L), pathological conditions, such as untreated diabetes and ketoacidosis, occur. The figure was created with BioRender.comCC BY-NC-ND · PubMed Central
Figure 3. Molecular Responses to Induction of Ketosis. Abbreviations: IL, interleukin; GPR109A, hydroxycarboxylic acid receptor 2, niacin receptor 1; MCFA, medium-chain fatty acid; NF-κB, nuclear factor–kappa B; NLR, Nod-like receptor protein family; NLRP3, NLR pyrin domain-containing protein 3; Nrf2, nuclear factor erythroid 2-related factor 2; ROS, reactive oxygen species; TNFα, tumor necrosis factor alpha; TLR4, Toll-like receptor 4. The figure was created with BioRender.com
Figure 3. Molecular Responses to Induction of Ketosis. Abbreviations: IL, interleukin; GPR109A, hydroxycarboxylic acid receptor 2, niacin receptor 1; MCFA, medium-chain fatty acid; NF-κB, nuclear factor–kappa B; NLR, Nod-like receptor protein family; NLRP3, NLR pyrin domain-containing protein 3; Nrf2, nuclear factor erythroid 2-related factor 2; ROS, reactive oxygen species; TNFα, tumor necrosis factor alpha; TLR4, Toll-like receptor 4. The figure was created with BioRender.comCC BY-NC-ND · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 26 references

Research works printed but not linked: 139

  1. Curran, 2023, Correlates of physical activity and sedentary behavior in adults living with overweight and obesity: a systematic review, Obes Rev, 24, e13615, 10.1111/obr.13615 · DOI
  2. Bray, 2016, Management of obesity, Lancet, 387, 1947, 10.1016/S0140-6736(16)00271-3 · DOI · Paper page
  3. Yoong, 2016, Systematic review and meta-analysis of interventions targeting sleep and their impact on child body mass index, diet, and physical activity, Obesity (Silver Spring), 24, 1140, 10.1002/oby.21459 · DOI
  4. van Baak, 2023, Obesity-induced and weight-loss-induced physiological factors affecting weight regain, Nat Rev Endocrinol, 19, 655, 10.1038/s41574-023-00887-4 · DOI
  5. Jaacks, 2019, The obesity transition: stages of the global epidemic, Lancet Diabetes Endocrinol, 7, 231, 10.1016/S2213-8587(19)30026-9 · DOI · Paper page
  6. Achamrah, 2018, Comparison of body composition assessment by DXA and BIA according to the body mass index: a retrospective study on 3655 measures, PLoS One, 13, e0200465, 10.1371/journal.pone.0200465 · DOI · Paper page
  7. Schnall, 2016, Globalization, work, and cardiovascular disease, Int J Health Serv, 46, 656, 10.1177/0020731416664687 · DOI
  8. Scherer, 2016, Obesity, diabetes, and cardiovascular diseases, Circ Res, 118, 1703, 10.1161/CIRCRESAHA.116.308999 · DOI · Paper page
  9. Beak, 2022, Predisposing factors for posttraumatic osteoarthritis after malleolus fracture fixation in patients younger than 50 years, Foot Ankle Int, 43, 389, 10.1177/10711007211050039 · DOI
  10. Hazlehurst, 2022, How to manage weight loss in women with obesity and PCOS seeking fertility?, Clin Endocrinol (Oxf), 97, 208, 10.1111/cen.14726 · DOI · Paper page
  11. Hunter, 2021, The effectiveness of weight-loss lifestyle interventions for improving fertility in women and men with overweight or obesity and infertility: a systematic review update of evidence from randomized controlled trials, Obes Rev, 22, e13325, 10.1111/obr.13325 · DOI
  12. Adnan, 2022, Body mass index and diabetes mellitus may predict poorer overall survival of oral squamous cell carcinoma patients: a retrospective cohort from a tertiary-care centre of a resource-limited country, Clin Med Insights Oncol, 16, 11795549221084832, 10.1177/11795549221084832 · DOI
  13. Bou Malhab, 2022, Obesity and inflammation: colorectal cancer engines, Curr Mol Pharmacol, 15, 620, 10.2174/1874467214666210906122054 · DOI
  14. Sakai, 2018, Obesity, metabolic disease and the pancreas—quantitative imaging of pancreatic fat, Br J Radiol, 91, 20180267, 10.1259/bjr.20180267 · DOI
  15. Luppino, 2010, Overweight, obesity, and depression, Arch Gen Psychiatry, 67, 220, 10.1001/archgenpsychiatry.2010.2 · DOI · Paper page
  16. Mazereel, 2020, Impact of psychotropic medication effects on obesity and the metabolic syndrome in people with serious mental illness, Front Endocrinol (Lausanne), 11, 573479, 10.3389/fendo.2020.573479 · DOI
  17. Lennerz, 2021, Carbohydrate restriction for diabetes: rediscovering centuries-old wisdom, J Clin Invest, 131, 10.1172/JCI142246 · DOI
  18. Cooder, 1933, Epilepsy in children: with particular reference to the ketogenic diet, Cal West Med, 39, 169
  19. IJff, 2016, Cognitive and behavioral impact of the ketogenic diet in children and adolescents with refractory epilepsy: a randomized controlled trial, Epilepsy Behav, 60, 153, 10.1016/j.yebeh.2016.04.033 · DOI
  20. Ros Pérez, 1989, Evaluation of the effectiveness of the ketogenic diet with medium-chain triglycerides, in the treatment of refractory epilepsy in children. Apropos of a series of cases, An Esp Pediatr, 30, 155
  21. Sandu, 2019, Ketogenic diet in patients with GLUT1 deficiency syndrome, Maedica (Bucur), 14, 93, 10.26574/maedica.2019.14.2.93 · DOI
  22. Institute of Medicine (US); Subcommittee on Interpretation and Uses of Dietary Reference Intakes; Institute of Medicine (US) Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, 2000, DRI Dietary Reference Intakes: Applications in Dietary Assessment, 10.17226/9956 · DOI
  23. Yalcin, 2017, The effects of meal glycemic load on blood glucose levels of adults with different body mass indexes, Indian J Endocrinol Metab, 21, 71, 10.4103/2230-8210.195995 · DOI
  24. Wallace, 2022, Obesity and dietary fat influence dopamine neurotransmission: exploring the convergence of metabolic state, physiological stress, and inflammation on dopaminergic control of food intake, Nutr Res Rev, 35, 236, 10.1017/S0954422421000196 · DOI
  25. Speakman, 2021, Carbohydrates, insulin, and obesity, Science, 372, 577, 10.1126/science.aav0448 · DOI
  26. Schugar, 2012, Low-carbohydrate ketogenic diets, glucose homeostasis, and nonalcoholic fatty liver disease, Curr Opin Clin Nutr Metab Care, 15, 374, 10.1097/MCO.0b013e3283547157 · DOI
  27. Spriet, 2014, New insights into the interaction of carbohydrate and fat metabolism during exercise, Sports Med, 44(Suppl 1), S87, 10.1007/s40279-014-0154-1 · DOI · Paper page
  28. Shah, 2020, Tracking the carbons supplying gluconeogenesis, J Biol Chem, 295, 14419, 10.1074/jbc.REV120.012758 · DOI
  29. Lilly, 2019, The effect of added peanut butter on the glycemic response to a high–glycemic index meal: a pilot study, J Am Coll Nutr, 38, 351, 10.1080/07315724.2018.1519404 · DOI
  30. Li, 2015, Saturated fats compared with unsaturated fats and sources of carbohydrates in relation to risk of coronary heart disease: a prospective cohort study, J Am Coll Cardiol, 66, 1538, 10.1016/j.jacc.2015.07.055 · DOI · Paper page
  31. Lemeshow, 2018, Food and beverage consumption and food addiction among women in the Nurses’ Health Studies, Appetite, 121, 186, 10.1016/j.appet.2017.10.038 · DOI
  32. Jaworowska, 2013, Nutritional challenges and health implications of takeaway and fast food, Nutr Rev, 71, 310, 10.1111/nure.12031 · DOI
  33. Lovejoy, 2002, Effects of diets enriched in saturated (palmitic), monounsaturated (oleic), or trans (elaidic) fatty acids on insulin sensitivity and substrate oxidation in healthy adults, Diabetes Care, 25, 1283, 10.2337/diacare.25.8.1283 · DOI
  34. Oteng, 2020, Mechanisms of action of trans fatty acids, Adv Nutr, 11, 697, 10.1093/advances/nmz125 · DOI
  35. Zhu, 2024, Associations between trans fatty acids and systemic immune-inflammation index: a cross-sectional study, Lipids Health Dis, 23, 122, 10.1186/s12944-024-02109-w · DOI
  36. Wanders, 2010, Effect of a high intake of conjugated linoleic acid on lipoprotein levels in healthy human subjects, PLoS One, 5, e9000, 10.1371/journal.pone.0009000 · DOI
  37. Matthan, 2024, Effect of daily avocado consumption for 6 mo compared with habitual diet on red blood cell fatty acid profiles and association with cardiometabolic risk factors in individuals with abdominal obesity: a randomized trial, Am J Clin Nutr, 120, 794, 10.1016/j.ajcnut.2024.08.002 · DOI
  38. Mann, 1994, Metabolic consequences of dietary trans fatty acids, Lancet, 343, 1268, 10.1016/s0140-6736(94)92157-1 · DOI
  39. Scholz, 2019, Association between trans fatty acid intake and overweight including obesity in 4 to 5-year-old children from the INMA study, Pediatr Obes, 14, e12528, 10.1111/ijpo.12528 · DOI
  40. Sun, 2019, Differential effects of monounsaturated and polyunsaturated fats on satiety and gut hormone responses in healthy subjects, Foods, 8, 634, 10.3390/foods8120634 · DOI
  41. Stevenson, 2017, Hunger and satiety responses to high-fat meals after a high-polyunsaturated fat diet: a randomized trial, Nutrition, 41, 14, 10.1016/j.nut.2017.03.008 · DOI
  42. Fukao, 2004, Pathways and control of ketone body metabolism: on the fringe of lipid biochemistry, Prostaglandins Leukot Essent Fatty Acids, 70, 243, 10.1016/j.plefa.2003.11.001 · DOI
  43. Nelson, 2023, Metabolic messengers: ketone bodies, Nat Metab, 5, 2062, 10.1038/s42255-023-00935-3 · DOI
  44. Dąbek, 2020, Modulation of cellular biochemistry, epigenetics and metabolomics by ketone bodies. Implications of the ketogenic diet in the physiology of the organism and pathological states, Nutrients, 12, 788, 10.3390/nu12030788 · DOI
  45. Huang, 2011, Circadian rhythms, sleep, and metabolism, J Clin Invest, 121, 2133, 10.1172/JCI46043 · DOI
  46. Owen, 1969, Liver and kidney metabolism during prolonged starvation, J Clin Invest, 48, 574, 10.1172/JCI106016 · DOI
  47. Jensen, 2011, The role of skeletal muscle glycogen breakdown for regulation of insulin sensitivity by exercise, Front Physiol, 2, 112, 10.3389/fphys.2011.00112 · DOI · Paper page
  48. Mikkelsen, 2015, Systemic, cerebral and skeletal muscle ketone body and energy metabolism during acute hyper-D-β-hydroxybutyratemia in post-absorptive healthy males, J Clin Endocrinol Metab, 100, 636, 10.1210/jc.2014-2608 · DOI
  49. Fery, 1988, Effect of exercise on the disposal of infused ketone bodies in humans, J Clin Endocrinol Metab, 67, 245, 10.1210/jcem-67-2-245 · DOI
  50. Balasse, 1989, Ketone body production and disposal: effects of fasting, diabetes, and exercise, Diabetes Metab Rev, 5, 247, 10.1002/dmr.5610050304 · DOI
  51. Pedroso, 2014, Leucine improves protein nutritional status and regulates hepatic lipid metabolism in calorie-restricted rats, Cell Biochem Funct, 32, 326, 10.1002/cbf.3017 · DOI
  52. Harvey, 2018, The use of nutritional supplements to induce ketosis and reduce symptoms associated with keto-induction: a narrative review, PeerJ, 6, e4488, 10.7717/peerj.4488 · DOI
  53. Harvey, 2018, The effect of medium chain triglycerides on time to nutritional ketosis and symptoms of keto-induction in healthy adults: a randomised controlled clinical trial, J Nutr Metab, 2018, 2630565, 10.1155/2018/2630565 · DOI
  54. Jensen, 2020, Effects of ketone bodies on brain metabolism and function in neurodegenerative diseases, Int J Mol Sci, 21, 8767, 10.3390/ijms21228767 · DOI
  55. Stubbs, 2017, On the metabolism of exogenous ketones in humans, Front Physiol, 8, 848, 10.3389/fphys.2017.00848 · DOI
  56. Poff, 2020, Nutritional ketosis with ketogenic diets or exogenous ketones: features, convergence, and divergence, Curr Sports Med Rep, 19, 251, 10.1249/JSR.0000000000000732 · DOI
  57. Soto-Mota, 2019, Safety and tolerability of sustained exogenous ketosis using ketone monoester drinks for 28 days in healthy adults, Regul Toxicol Pharmacol, 109, 104506, 10.1016/j.yrtph.2019.104506 · DOI · Paper page
  58. Walsh, 2021, 14-Day ketone supplementation lowers glucose and improves vascular function in obesity: a randomized crossover trial, J Clin Endocrinol Metab, 106, 1738, 10.1210/clinem/dgaa925 · DOI
  59. Maalouf, 2009, The neuroprotective properties of calorie restriction, the ketogenic diet, and ketone bodies, Brain Res Rev, 59, 293, 10.1016/j.brainresrev.2008.09.002 · DOI
  60. Yang, 1976, Composition of weight lost during short-term weight reduction. Metabolic responses of obese subjects to starvation and low-calorie ketogenic and nonketogenic diets, J Clin Invest, 58, 722, 10.1172/JCI108519 · DOI
  61. Lennerz, 2018, Management of type 1 diabetes with a very low–carbohydrate diet, Pediatrics, 142, 10.1542/peds.2017-3349 · DOI
  62. Bueno, 2013, Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomised controlled trials, Br J Nutr, 110, 1178, 10.1017/S0007114513000548 · DOI · Paper page
  63. Liu, 2008, Medium-chain triglyceride (MCT) ketogenic therapy, Epilepsia, 49(Suppl 8), 33, 10.1111/j.1528-1167.2008.01830.x · DOI
  64. Vidić, 2021, Effects of calorie restricted low carbohydrate high fat ketogenic vs. non-ketogenic diet on strength, body-composition, hormonal and lipid profile in trained middle-aged men, Clin Nutr, 40, 1495, 10.1016/j.clnu.2021.02.028 · DOI
  65. Kysel, 2020, The influence of cyclical ketogenic reduction diet vs. nutritionally balanced reduction diet on body composition, strength, and endurance performance in healthy young males: a randomized controlled trial, Nutrients, 12, 2832, 10.3390/nu12092832 · DOI
  66. Zoccali, 2023, The effect of a ketogenic diet on weight loss in CKD: a randomized controlled trial in obese stage G1-3a CKD patients, Clin Kidney J, 16, 2309, 10.1093/ckj/sfad176 · DOI
  67. Basciani, 2020, Very-low-calorie ketogenic diets with whey, vegetable, or animal protein in patients with obesity: a randomized pilot study, J Clin Endocrinol Metab, 105, 10.1210/clinem/dgaa336 · DOI
  68. Molteberg, 2023, Stress biomarkers in adult patients with drug-resistant epilepsy on a modified Atkins diet: a prospective study, Epilepsia Open, 8, 1331, 10.1002/epi4.12808 · DOI
  69. Gibson, 2015, Do ketogenic diets really suppress appetite? A systematic review and meta-analysis, Obes Rev, 16, 64, 10.1111/obr.12230 · DOI · Paper page
  70. Hession, 2009, Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities, Obes Rev, 10, 36, 10.1111/j.1467-789X.2008.00518.x · DOI
  71. Mohler, 2013, Endothelial function and weight loss: comparison of low-carbohydrate and low-fat diets, Obesity (Silver Spring), 21, 504, 10.1002/oby.20055 · DOI
  72. Arora, 2023, Intermittent fasting with ketogenic diet: a combination approach for management of chronic diseases, Clin Nutr ESPEN, 54, 166, 10.1016/j.clnesp.2023.01.024 · DOI
  73. Ganesan, 2018, Intermittent fasting: the choice for a healthier lifestyle, Cureus, 10, e2947, 10.7759/cureus.2947 · DOI
  74. Harvie, 2013, The effect of intermittent energy and carbohydrate restriction v. daily energy restriction on weight loss and metabolic disease risk markers in overweight women, Br J Nutr, 110, 1534, 10.1017/S0007114513000792 · DOI · Paper page
  75. Gangitano, 2021, Chronobiology and metabolism: is ketogenic diet able to influence circadian rhythm?, Front Neurosci, 15, 756970, 10.3389/fnins.2021.756970 · DOI
  76. Blanco, 2019, Starvation ketoacidosis due to the ketogenic diet and prolonged fasting—a possibly dangerous diet trend, Am J Case Rep, 20, 1728, 10.12659/AJCR.917226 · DOI
  77. Conklin, 1922, Cause and treatment of epilepsy, J Am Osteopathic Assoc, 26, 11
  78. Wheless, 2008, History of the ketogenic diet, Epilepsia, 49(Suppl 8), 3, 10.1111/j.1528-1167.2008.01821.x · DOI
  79. Sampaio, 2016, Ketogenic diet for epilepsy treatment, Arq Neuropsiquiatr, 74, 842, 10.1590/0004-282X20160116 · DOI
  80. Keith, 2021, Ketogenic diet as a potential intervention for lipedema, Med Hypotheses, 146, 110435, 10.1016/j.mehy.2020.110435 · DOI
  81. Tchernof, 2013, Pathophysiology of human visceral obesity: an update, Physiol Rev, 93, 359, 10.1152/physrev.00033.2011 · DOI · Paper page
  82. Ballak, 2015, IL-1 family members in the pathogenesis and treatment of metabolic disease: focus on adipose tissue inflammation and insulin resistance, Cytokine, 75, 280, 10.1016/j.cyto.2015.05.005 · DOI
  83. Frayn, 2003, Integrative physiology of human adipose tissue, Int J Obes Relat Metab Disord, 27, 875, 10.1038/sj.ijo.0802326 · DOI
  84. Hall, 2015, Obesity-induced hypertension, Circ Res, 116, 991, 10.1161/CIRCRESAHA.116.305697 · DOI · Paper page
  85. Benjamin, 2018, Heart disease and stroke statistics—2018 update: a report from the American Heart Association, Circulation, 137, e67, 10.1161/CIR.0000000000000558 · DOI · Paper page
  86. Shariq, 2020, Obesity-related hypertension: a review of pathophysiology, management, and the role of metabolic surgery, Gland Surg, 9, 80, 10.21037/gs.2019.12.03 · DOI
  87. Abdul Kadir, 2020, Cardiac ketone body metabolism, Biochim Biophys Acta Mol Basis Dis, 1866, 165739, 10.1016/j.bbadis.2020.165739 · DOI
  88. Cotter, 2013, Ketone body metabolism and cardiovascular disease, Am J Physiol Heart Circ Physiol, 304, H1060, 10.1152/ajpheart.00646.2012 · DOI
  89. Aubert, 2016, The failing heart relies on ketone bodies as a fuel, Circulation, 133, 698, 10.1161/CIRCULATIONAHA.115.017355 · DOI
  90. Yurista, 2021, Therapeutic potential of ketone bodies for patients with cardiovascular disease, J Am Coll Cardiol, 77, 1660, 10.1016/j.jacc.2020.12.065 · DOI
  91. Takahara, 2022, Ketone therapy for heart failure: current evidence for clinical use, Cardiovasc Res, 118, 977, 10.1093/cvr/cvab068 · DOI
  92. Pirola, 2022, Fat not so bad? The role of ketone bodies and ketogenic diet in the treatment of endothelial dysfunction and hypertension, Biochem Pharmacol, 206, 115346, 10.1016/j.bcp.2022.115346 · DOI
  93. Tzenios, 2022, Examining the efficacy of a very-low-carbohydrate ketogenic diet on cardiovascular health in adults with mildly elevated low-density lipoprotein cholesterol in an open-label pilot study, Metab Syndr Relat Disord, 20, 94, 10.1089/met.2021.0042 · DOI
  94. Guh, 2009, The incidence of co-morbidities related to obesity and overweight: a systematic review and meta-analysis, BMC Public Health, 9, 88, 10.1186/1471-2458-9-88 · DOI · Paper page
  95. Cashen, 2019, Diabetic ketoacidosis, Pediatr Rev, 40, 412, 10.1542/pir.2018-0231 · DOI
  96. Dhatariya, 2019, Defining and characterising diabetic ketoacidosis in adults, Diabetes Res Clin Pract, 155, 107797, 10.1016/j.diabres.2019.107797 · DOI
  97. Tallis, 2018, The effects of obesity on skeletal muscle contractile function, J Exp Biol, 221, 16384, 10.1242/jeb.163840 · DOI
  98. Napoli, 2017, Mechanisms of diabetes mellitus-induced bone fragility, Nat Rev Endocrinol, 13, 208, 10.1038/nrendo.2016.153 · DOI · Paper page
  99. Iyer, 2010, Inflammatory lipid mediators in adipocyte function and obesity, Nat Rev Endocrinol, 6, 71, 10.1038/nrendo.2009.264 · DOI
  100. Bliddal, 2014, Osteoarthritis, obesity and weight loss: evidence, hypotheses and horizons—a scoping review, Obes Rev, 15, 578, 10.1111/obr.12173 · DOI · Paper page
  101. King, 2013, Obesity & osteoarthritis, Indian J Med Res, 138, 185
  102. Zapata-Linares, 2021, Role of adipose tissues in osteoarthritis, Curr Opin Rheumatol, 33, 84, 10.1097/BOR.0000000000000763 · DOI · Paper page
  103. Fan, 2021, Causal association of adipokines with osteoarthritis: a Mendelian randomization study, Rheumatology (Oxford), 60, 2808, 10.1093/rheumatology/keaa719 · DOI
  104. Mathus-Vliegen, 2012, Prevalence, pathophysiology, health consequences and treatment options of obesity in the elderly: a guideline, Obes Facts, 5, 460, 10.1159/000341193 · DOI · Paper page
  105. Babu, 2021, Can intermittent fasting be helpful for knee osteoarthritis?, J Clin Orthop Trauma, 16, 70, 10.1016/j.jcot.2020.12.020 · DOI
  106. Muthuri, 2011, What if we prevent obesity? Risk reduction in knee osteoarthritis estimated through a meta-analysis of observational studies, Arthritis Care Res (Hoboken), 63, 982, 10.1002/acr.20464 · DOI
  107. Drinda, 2018, AGE-RAGE interaction does not explain the clinical improvements after therapeutic fasting in osteoarthritis, Complement Med Res, 25, 167, 10.1159/000486237 · DOI
  108. Strath, 2020, The effect of low-carbohydrate and low-fat diets on pain in individuals with knee osteoarthritis, Pain Med, 21, 150, 10.1093/pm/pnz022 · DOI
  109. Masino, 2013, Ketogenic diets and pain, J Child Neurol, 28, 993, 10.1177/0883073813487595 · DOI
  110. Marques Miranda, 2021, Diet, body weight and pain susceptibility—a systematic review of preclinical studies, Neurobiol Pain, 10, 100066, 10.1016/j.ynpai.2021.100066 · DOI
  111. Felson, 2021, Fatty acids and osteoarthritis: the MOST study, Osteoarthritis Cartilage, 29, 973, 10.1016/j.joca.2021.03.006 · DOI
  112. Fraser, 2000, Reduction in serum leptin and IGF-1 but preserved T-lymphocyte numbers and activation after a ketogenic diet in rheumatoid arthritis patients, Clin Exp Rheumatol, 18, 209
  113. Fraser, 2000, Serum levels of interleukin-6 and dehydroepiandrosterone sulphate in response to either fasting or a ketogenic diet in rheumatoid arthritis patients, Clin Exp Rheumatol, 18, 357
  114. Barber, 2019, Obesity and polycystic ovary syndrome: implications for pathogenesis and novel management strategies, Clin Med Insights Reprod Health, 13, 1179558119874042, 10.1177/1179558119874042 · DOI · Paper page
  115. Li, 2021, Ketogenic diet in women with polycystic ovary syndrome and liver dysfunction who are obese: a randomized, open-label, parallel-group, controlled pilot trial, J Obstet Gynaecol Res, 47, 1145, 10.1111/jog.14650 · DOI
  116. Kulak, 2013, Should the ketogenic diet be considered for enhancing fertility?, Maturitas, 74, 10, 10.1016/j.maturitas.2012.10.003 · DOI
  117. Ye, 2018, Subversion of systemic glucose metabolism as a mechanism to support the growth of leukemia cells, Cancer Cell, 34, 659, 10.1016/j.ccell.2018.08.016 · DOI
  118. Zhang, 2018, Low ketolytic enzyme levels in tumors predict ketogenic diet responses in cancer cell lines in vitro and in vivo, J Lipid Res, 59, 625, 10.1194/jlr.M082040 · DOI
  119. Feng, 2019, Multi-dimensional roles of ketone bodies in cancer biology: opportunities for cancer therapy, Pharmacol Res, 150, 104500, 10.1016/j.phrs.2019.104500 · DOI
  120. Lin, 2013, Dietary restriction suppresses tumor growth, reduces angiogenesis, and improves tumor microenvironment in human non-small-cell lung cancer xenografts, Lung Cancer, 79, 111, 10.1016/j.lungcan.2012.11.001 · DOI
  121. Allen, 2013, Ketogenic diets enhance oxidative stress and radio-chemo-therapy responses in lung cancer xenografts, Clin Cancer Res, 19, 3905, 10.1158/1078-0432.CCR-12-0287 · DOI
  122. Woolf, 2016, Tumor metabolism, the ketogenic diet and β-hydroxybutyrate: novel approaches to adjuvant brain tumor therapy, Front Mol Neurosci, 9, 122, 10.3389/fnmol.2016.00122 · DOI
  123. Zuccoli, 2010, Metabolic management of glioblastoma multiforme using standard therapy together with a restricted ketogenic diet: case Rrport, Nutr Metab (Lond), 7, 33, 10.1186/1743-7075-7-33 · DOI
  124. Hao, 2015, Growth of human colon cancer cells in nude mice is delayed by ketogenic diet with or without omega-3 fatty acids and medium-chain triglycerides, Asian Pac J Cancer Prev, 16, 2061, 10.7314/APJCP.2015.16.5.2061 · DOI
  125. Cohen, 2020, A ketogenic diet is acceptable in women with ovarian and endometrial cancer and has no adverse effects on blood lipids: a randomized, controlled trial, Nutr Cancer, 72, 584, 10.1080/01635581.2019.1645864 · DOI
  126. Cohen, 2018, Favorable effects of a ketogenic diet on physical function, perceived energy, and food cravings in women with ovarian or endometrial cancer: a randomized, controlled trial, Nutrients, 10, 1187, 10.3390/nu10091187 · DOI
  127. Cohen, 2018, A ketogenic diet reduces central obesity and serum insulin in women with ovarian or endometrial cancer, J Nutr, 148, 1253, 10.1093/jn/nxy119 · DOI
  128. Porper, 2021, Dietary-induced ketogenesis: adults are not children, Nutrients, 13, 3093, 10.3390/nu13093093 · DOI
  129. Chu-Shore, 2010, Tumor growth in patients with tuberous sclerosis complex on the ketogenic diet, Brain Dev, 32, 318, 10.1016/j.braindev.2009.04.009 · DOI
  130. Zahra, 2017, Consuming a ketogenic diet while receiving radiation and chemotherapy for locally advanced lung cancer and pancreatic cancer: the University of Iowa experience of two phase 1 clinical trials, Radiat Res, 187, 743, 10.1667/RR14668.1 · DOI
  131. Tragni, 2021, Reduction of cardio-metabolic risk and body weight through a multiphasic very-low calorie ketogenic diet program in women with overweight/obesity: a study in a real-world setting, Nutrients, 13, 1804, 10.3390/nu13061804 · DOI
  132. Arslan, 2016, Is ketogenic diet treatment hepatotoxic for children with intractable epilepsy?, Seizure, 43, 32, 10.1016/j.seizure.2016.10.024 · DOI
  133. Vargas-Molina, 2024, The effect of the ketogenic diet on resistance training load management: a repeated-measures clinical trial in trained participants, J Int Soc Sports Nutr, 21, 2306308, 10.1080/15502783.2024.2306308 · DOI
  134. Cho, 2023, The effect of a short-term ketogenic diet on exercise efficiency during graded exercise in healthy adults, J Int Soc Sports Nutr, 20, 2264278, 10.1080/15502783.2023.2264278 · DOI
  135. McKay, 2020, Iron metabolism: interactions with energy and carbohydrate availability, Nutrients, 12, 3692, 10.3390/nu12123692 · DOI · Paper page
  136. Li, 2023, Effects of a two meals-a-day ketogenic diet on newly diagnosed obese patients with type 2 diabetes mellitus: a retrospective observational study, Medicine (Baltimore), 102, E 35753, 10.1097/MD.0000000000035753 · DOI
  137. Watanabe, 2020, Scientific evidence underlying contraindications to the ketogenic diet: an update, Obes Rev, 21, E13053, 10.1111/obr.13053 · DOI
  138. Graybeal, 2024, Changes in the chronic and postprandial blood lipid profiles of trained competitive cyclists and triathletes following a ketogenic diet: a randomized crossover trial, BMC Sports Sci Med Rehabil, 16, 19, 10.1186/s13102-023-00801-5 · DOI
  139. Berry-Kravis, 2001, Carnitine levels and the ketogenic diet, Epilepsia, 42, 1445, 10.1046/j.1528-1157.2001.18001.x · DOI

Cited by

Sorted by citations

See all 18

Metadata

Authors
Biesiekierska, M., Strigini, M., Śliwińska, A., Pirola, L., & Balcerczyk, A.
Affiliations
  • Department of Oncobiology and Epigenetics, Faculty of Biology and Environmental Protection, University of Lodz , 90-236 Lodz,
  • University Jean Monnet Saint-Etienne, INSERM, Mines Saint Etienne, SAINBIOSE U1059 , F-42023 Saint-Etienne,
  • Department of Nucleic Acid Biochemistry, Medical University of Lodz , 92-213 Lodz,
  • INSERM Unit 1060, CarMeN Laboratory, Lyon 1 University , F-69495 Pierre Bénite,
ORCID
Pirola, Luciano
Venue
Nutrition Reviews
Publisher
Oxford University Press (OUP)
Published
2025-02-26
Volume
83
Issue
10
Pages
1957-1972
ISSN
  • 0029-6643
  • 1753-4887
DOI
10.1093/nutrit/nuaf010
PMC
PMC12422014
Cited by
18
References
26
Language
en
Licence
creativecommons.org/licenses/by-nc-nd/4.0/ (vor)
Funders
  • Polish National Science Centre (2018/30/M/NZ3/00682)
  • University Jean Monnet
  • Saint-Etienne and INSERM
  • AAP 2017 of UJM Saint-Etienne
  • French Rheumatology Society (SFR 2020)
  • 2021 EFSD-Boehringer Ingelheim

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: The Impact of Ketogenic Nutrition on Obesity and Metabolic Health: Mechanisms and Clinical Implications. https://app.cochat.ai/papers/10.1093/nutrit/nuaf010
The paper
Biesiekierska, M., Strigini, M., Śliwińska, A., Pirola, L., & Balcerczyk, A. (2025). The Impact of Ketogenic Nutrition on Obesity and Metabolic Health: Mechanisms and Clinical Implications. Nutrition Reviews. https://doi.org/10.1093/nutrit/nuaf010