HORMONES 2016, 15(4):572-573
DOI: 10.14310/horm.2002.1713
Letter to the Editor
Postprandial dysmetabolism: assessment and treatment
Niki Katsiki1, Genovefa Kolovou2

1Second Propedeutic Department of Internal Medicine, Medical School, Aristotle University of Thessaloniki, Hippocration Hospital, Thessaloniki, Greece; 2Cardiology Departmentand Molecular Immunology Laboratory, Onassis Cardiac Surgery Center Athens, Greece

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We read with interest the Pappas et al review on postprandial dysmetabolism.1 The authors describe evidence linking elevated levels of postprandial glucose and triglycerides (TGs) with cardiovascular (CV) morbidity and mortality as well as with polycystic ovary syndrome (PCOS), non-alcoholic fatty liver disease (NAFLD) and lack of hepatic receptors such as low density lipoprotein receptor (LDLR).1 Specifically, it was reported that subjects with familial hypercholesterolemia have exaggerated and prolonged response to fatty meal loading.2 The authors also discuss methods for screening and diagnosis of postprandial dysmetabolism as well as therapeutic options including lifestyle modifications, antidiabetic and hypolipidemic drugs.

The lack of a widely approved standardized protocol for the assessment of postprandial lipemia (PPL) impedes the early diagnosis and adequate treatment of this metabolic disorder.3 In this context, a previous meta-analysis proposeda 4 h time-point following an oral fat test meal containing 70-79 g of fat as the most representative method to measure PPL.4 Pappas et al.1mention the cut-off point of 175 mg/dl for non-fasting TGs as suggested by White et al5 in a sub-population of the Women’s Health Study. An expert panel statement had earlier discussed the clinical implications and assessment of PPL proposing as optimal non-fasting TGs <180 mg/dl (2 mmol/l) and desirable postprandial TGs ≤220 mg/dl (2.5 mmol/l) at any time following a fat tolerance test (given after 8 h of fasting and consisting of 75 g fat, 25 g carbohydrates and 10 g protein).6 The same expert panel recommended that a fat tolerance test should be performed in individuals with non-fasting TGs 89-180 md/dl (1-2 mmol/l).

Antidiabetic and hypolipidemic drugs have been reported to improve postprandial dysmetabolism as mentioned by Pappas et al.1 Statins and insulin-sensitizer drugs (i.e. metformin and pioglitazone) were also shown to beneficially affect metabolic and menstrual abnormalities in PCOS.7 Moreover, it was found that gut peptides such as glucagon-like peptide-1 (GLP-1) and GLP-2 could be involved in homeostasis of PPL. Thus, the GLP-1 receptor agonists (GLP-1 RA) may be able to improve metabolic features in PCOS women but further research is needed in this field.8 With regard to NAFLD, statins and antidiabetic drugs [e.g. pioglitazone, dipeptidyl peptidase-4 (DPP-4) inhibitors, GLP-1 RA and sodium-glucose co-transporter 2 (SGLT2) inhibitors] are also likely to improve biochemical and/or histological features of NAFLD and its advanced form i.e. non-alcoholic steatohepatitis (NASH).9-13 Overall, combination therapy with both antidiabetic and hypolipidemic drugs may be a useful therapeutic tool for patients with postprandial dysmetabolism and PCOS or NAFLD.14-16 Nevertheless, further  investigations are required to firmly establish such associations.


This letter was written independently; no company or institution supported it financially. NK has given talks, attended conferences and participated in trials sponsored by Amgen, Angelini, AstraZeneca, Boehringer Ingelheim, MSD, Novartis, Novo Nordisk and Sanofi-Aventis. GK has given talks, attended conferences and participated in trials sponsored by Amgen, Angelini, MSD, Lilly, Vianex and Sanofi-Aventis.


1. Pappas C, Kandaraki EA, Tsirona S, Kountouras D, Kassi G, Diamanti-Kandarakis E, 2016 Postprandial dysmetabolism: Too early or too late? Hormones (Athens) 15: 321-344.
2. Kolovou GD, Kostakou PM, Anagnostopoulou KK, 2011 Familial hypercholesterolemia and triglyceride metabolism. Int J Cardiol 147: 349-358.
3. Kolovou GD, Mikhailidis DP, Kovar J, et al, 2011 Assessment and clinical relevance of non-fasting and postprandial triglycerides: an expert panel statement. Curr Vasc Pharmacol 9: 258-270.
4. Mihas C, Kolovou GD, Mikhailidis DP, et al, 2011 Diagnostic value of postprandial triglyceride testing in healthy subjects: a meta-analysis. Curr Vasc Pharmacol 9: 271-280.
5. White KT, Moorthy MV, Akinkuolie AO, et al, 2015 Identifying an optimal cutpoint for the diagnosis of hypertriglyceridemia in the nonfasting state. Clin Chem 61: 1156-1163.
6. Kolovou GD, Mikhailidis DP, Nordestgaard BG, Bilianou H, Panotopoulos G, 2011 Definition of postprandial lipaemia. Curr Vasc Pharmacol 9: 292-301.
7. Spritzer PM, Motta AB, Sir-Petermann T, Diamanti-Kandarakis E, 2015 Novel strategies in the management of polycystic ovary syndrome. Minerva Endocrinol 40: 195-212.
8. Tzotzas T, Karras SN, Katsiki N, 2016 Glucagon-like peptide-1 (GLP-1) receptor agonists in the treatment of obese women with polycystic ovary syndrome. Curr Vasc Pharmacol Dec 21. [Epub ahead of print].
9. Athyros VG, Katsiki N, Karagiannis A, Mikhailidis DP, 2013 Statins and non-alcoholic fatty liver disease: a bright future? Expert Opin Investig Drugs 22: 1089-1093.
10. Athyros VG, Katsiki N, Karagiannis A, 2016 Editorial: can glucagon like peptide 1 (GLP1) agonists or sodium-glucose co-transporter 2 (SGLT2) inhibitors ameliorate non-alcoholic steatohepatitis in people with or without diabetes? Curr Vasc Pharmacol 14: 494-497.
11. Musso G, Cassader M, Rosina F, Gambino R, 2012 Impact of current treatments on liver disease, glucose metabolism and cardiovascular risk in non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of randomized trials. Diabetologia 55: 885-904.
12. Blaslov K, Bulum T, Zibar K, Duvnjak L, 2014 Incretin based therapies: a novel treatment approach for non-alcoholic fatty liver disease. World J Gastroenterol 20: 7356-7365.
13. Katsiki N, Mikhailidis DP, Mantzoros CS, 2016 Non-alcoholic fatty liver disease and dyslipidemia: An update. Metabolism 65: 1109-1123.
14. Athyros VG, Katsiki N, Mikhailidis DP, 2016 Editorial: resolution of non-alcoholic-steatohepatitis. More than one drug needed? Curr Vasc Pharmacol 14: 313-315.
15. Sun J, Yuan Y, Cai R, et al, 2015 An investigation into the therapeutic effects of statins with metformin on polycystic ovary syndrome: a meta-analysis of randomised controlled trials. BMJ Open 5: e007280.
16. Katsiki N, Athyros VG, Mikhailidis DP, 2016 Non-alcoholic fatty liver disease in patients with type 2 diabetes mellitus: effects of statins and antidiabetic drugs. J Diabetes Complications. [Epub ahead of print].

Address for correspondence:
Genovefa D. Kolovou, MD, PhD, FESC, SFASA, FRSPH, Director, Cardiology Department, Lipid Disorders Clinic, Onassis Cardiac Surgery Center, 356 Sygrou Ave, 176 74, Athens, Greece; Tel.: +30 210 9493520, Fax: +30 210 9493336, E-mail: genovefa@kolovou.com

Received: 20-11-2016, Accepted: 26-11-2016