Skip to main content

Advertisement

SpringerLink
Log in

Acute Changes in Non-esterified Fatty Acids in Patients with Type 2 Diabetes Receiving Bariatric Surgery

  • Original Contributions
  • Published:
Obesity Surgery Aims and scope Submit manuscript

Abstract

Background

The purpose of this study was to compare acute changes of non-esterified fatty acids (NEFA) in relation to beta cell function (BCF) and insulin resistance in obese patients with type 2 diabetes (T2D) who underwent laparoscopic gastric bypass (GBP), laparoscopic sleeve gastrectomy (SG) or very low calorie diet (VLCD).

Methods

In a non-randomised study, fasting plasma samples were collected from 38 obese patients with T2D, matched for age, body mass index (BMI) and glycaemic control, who underwent GBP (11) or SG (14) or VLCD (13). Samples were collected the day before and 3 days after the intervention, during a 75-g oral glucose tolerance test. Glucose, insulin, c-peptide, glucagon like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) were measured, and individual NEFAs were measured using a triple-quadrupole liquid chromatography-mass spectrometry (LC-MS/MS). BCF by mathematical modelling and insulin resistance were estimated.

Results

Palmitic acid significantly decreased after each intervention. Monounsaturated/polyunsaturated ratio (MUFA/PUFA) and unsaturated/saturated fat ratios increased after each intervention. BCF was improved only after VLCD. Linoleic acid was positively correlated with total insulin secretion (p = 0.03). Glucose sensitivity correlated with palmitic acid (p = 0.01), unsaturated/saturated ratio (p = 0.0008) and MUFA/PUFA (p = 0.009). HOMA-IR correlated with stearic acid (p = 0.03), unsaturated/saturated ratio (p = 0.005) and MUFA/PUFA (p = 0.009). GIP AUC0–120 correlated with stearic acid (p = 0.04), but not GLP-1.

Conclusions

GBP, SG and VLCD have similar acute effects on decreasing palmitic acid. Several NEFAs correlated with BCF parameters and HOMA-IR.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Fig. 1

Similar content being viewed by others

References

  1. Abbasi F, McLaughlin T, Lamendola C, et al. Insulin regulation of plasma free fatty acid concentrations is abnormal in healthy subjects with muscle insulin resistance. Metabolism. 2000;49(2):151–4.

    Article  CAS  PubMed  Google Scholar 

  2. McLaughlin T, Abbasi F, Lamendola C, et al. Metabolic changes following sibutramine-assisted weight loss in obese individuals: role of plasma free fatty acids in the insulin resistance of obesity. Metabolism. 2001;50(7):819–24.

    Article  CAS  PubMed  Google Scholar 

  3. Boden G. Role of fatty acids in the pathogenesis of insulin resistance and NIDDM. Diabetes. 1997;46(1):3–10.

    Article  CAS  PubMed  Google Scholar 

  4. Boden G. Obesity and free fatty acids. Endocrinol Metab Clin N Am. 2008;37(3):635–46.

    Article  CAS  Google Scholar 

  5. Vessby B. Dietary fat, fatty acid composition in plasma and the metabolic syndrome. Curr Opin Lipidol. 2003;14(1):15–9.

    Article  CAS  PubMed  Google Scholar 

  6. Large V, Peroni O, Letexier D, et al. Metabolism of lipids in human white adipocyte. Diabetes & metabolism. 2004;30(4):294–309.

    Article  CAS  Google Scholar 

  7. Stumvoll M, Jacob S. Multiple sites of insulin resistance: muscle, liver and adipose tissue. Experimental and clinical endocrinology & diabetes: official journal, German Society of Endocrinology [and] German Diabetes Association. 1999;107(2):107.

    Article  CAS  Google Scholar 

  8. Carlson OD, David JD, Schrieder JM, et al. Contribution of nonesterified fatty acids to insulin resistance in the elderly with normal fasting but diabetic 2-hour postchallenge plasma glucose levels: the Baltimore Longitudinal Study of Aging. Metabolism. 2007;56(10):1444–51.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Kashyap S, Belfort R, Gastaldelli A, et al. A sustained increase in plasma free fatty acids impairs insulin secretion in nondiabetic subjects genetically predisposed to develop type 2 diabetes. Diabetes. 2003;52(10):2461–74.

    Article  CAS  PubMed  Google Scholar 

  10. Stumvoll M, Goldstein BJ, van Haeften TW. Type 2 diabetes: principles of pathogenesis and therapy. Lancet. 2005;365(9467):1333–46.

    Article  CAS  PubMed  Google Scholar 

  11. Plourde CÉ, Grenier-Larouche T, Caron-Dorval D, et al. Biliopancreatic diversion with duodenal switch improves insulin sensitivity and secretion through caloric restriction. Obesity. 2014;22(8):1838–46.

    Article  CAS  PubMed  Google Scholar 

  12. Lim E, Hollingsworth K, Aribisala B, et al. Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia. 2011;54(10):2506–14.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. Goldrick R, Hirsch J. Serial studies on the metabolism of human adipose tissue. II. Effects of caloric restriction and refeeding on lipogenesis, and the uptake and release of free fatty acids in obese and nonobese individuals. J Clin Investig. 1964;43(9):1793.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  14. Boden G. Effects of free fatty acids (FFA) on glucose metabolism: significance for insulin resistance and type 2 diabetes. Experimental and clinical endocrinology & diabetes: official journal, German Society of Endocrinology [and] German Diabetes Association. 2003;111(3):121–4.

    Article  CAS  Google Scholar 

  15. Kang Z, Deng Y, Zhou Y, et al. Pharmacological reduction of NEFA restores the efficacy of incretin-based therapies through GLP-1 receptor signalling in the beta cell in mouse models of diabetes. Diabetologia. 2013;56(2):423–33.

    Article  CAS  PubMed  Google Scholar 

  16. Karpe F, Dickmann JR, Frayn KN. Fatty acids, obesity, and insulin resistance: time for a reevaluation. Diabetes. 2011;60(10):2441–9.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  17. Buchwald H, Estok R, Fahrbach K, et al. Weight and type 2 diabetes after bariatric surgery: systematic review and meta-analysis. Am J Med. 2009;122(3):248–56. e5.

    Article  PubMed  Google Scholar 

  18. Kashyap SR, Gatmaitan P, Brethauer S, et al. Bariatric surgery for type 2 diabetes: weighing the impact for obese patients. Cleve Clin J Med. 2010;77(7):468–76.

    Article  PubMed  PubMed Central  Google Scholar 

  19. Klein S, Mittendorfer B, Eagon JC, et al. Gastric bypass surgery improves metabolic and hepatic abnormalities associated with nonalcoholic fatty liver disease. Gastroenterology. 2006;130(6):1564–72.

    Article  CAS  PubMed  Google Scholar 

  20. Risérus U, Willett WC, Hu FB. Dietary fats and prevention of type 2 diabetes. Prog Lipid Res. 2009;48(1):44–51.

    Article  PubMed  Google Scholar 

  21. Salinari S, Bertuzzi A, Asnaghi S, et al. First-phase insulin secretion restoration and differential response to glucose load depending on the route of administration in type 2 diabetic subjects after bariatric surgery. Diabetes Care. 2009;32(3):375–80.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  22. Matthews D, Hosker J, Rudenski A, et al. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28(7):412–9.

    Article  CAS  PubMed  Google Scholar 

  23. Matsuda M, DeFronzo RA. Insulin sensitivity indices obtained from oral glucose tolerance testing: comparison with the euglycemic insulin clamp. Diabetes Care. 1999;22(9):1462–70.

    Article  CAS  PubMed  Google Scholar 

  24. Stumvoll M, Gerich J. Clinical features of insulin resistance and beta cell dysfunction and the relationship to type 2 diabetes. Clin Lab Med. 2001;21(1):31–51.

    CAS  PubMed  Google Scholar 

  25. Mari A, Schmitz O, Gastaldelli A, et al. Meal and oral glucose tests for assessment of β-cell function: modeling analysis in normal subjects. American Journal of Physiology-Endocrinology and Metabolism. 2002;283(6):E1159–E66.

    Article  CAS  PubMed  Google Scholar 

  26. Mari A, Tura A, Gastaldelli A, et al. Assessing insulin secretion by modeling in multiple-meal tests role of potentiation. Diabetes. 2002;51(suppl 1):S221–S6.

    Article  CAS  PubMed  Google Scholar 

  27. Tura A, Mari A, Winzer C, et al. Impaired β-cell function in lean normotolerant former gestational diabetic women. Eur J Clin Investig. 2006;36(1):22–8.

    Article  CAS  Google Scholar 

  28. Santoro N, Caprio S, Giannini C, et al. Oxidized fatty acids: a potential pathogenic link between fatty liver and type 2 diabetes in obese adolescents? Antioxid Redox Signal. 2014;20(2):383–9.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  29. Toledo K, Aranda M, Asenjo S, et al. Unsaturated fatty acids and insulin resistance in childhood obesity. J Pediatr Endocrinol Metab. 2014;27(5–6):503–10.

    CAS  PubMed  Google Scholar 

  30. McGarry J, Dobbins R. Fatty acids, lipotoxicity and insulin secretion. Diabetologia. 1999;42(2):128–38.

    Article  CAS  PubMed  Google Scholar 

  31. Sako Y, Grill VE. A 48-hour lipid infusion in the rat time-dependently inhibits glucose-induced insulin secretion and B cell oxidation through a process likely coupled to fatty acid oxidation*. Endocrinology. 1990;127(4):1580–9.

    Article  CAS  PubMed  Google Scholar 

  32. Kelly A, Ryder J, Marlatt K, et al. Changes in inflammation, oxidative stress and adipokines following bariatric surgery among adolescents with severe obesity. Int J Obes. 2016;40:275–80.

  33. Murri M, García-Fuentes E, García-Almeida JM, et al. Changes in oxidative stress and insulin resistance in morbidly obese patients after bariatric surgery. Obes Surg. 2010;20(3):363–8.

    Article  PubMed  Google Scholar 

  34. Chait A, Kim F. Saturated fatty acids and inflammation: who pays the toll? Arterioscler Thromb Vasc Biol. 2010;30(4):692–3.

    Article  CAS  PubMed  Google Scholar 

  35. Ehses J, Meier D, Wueest S, et al. Toll-like receptor 2-deficient mice are protected from insulin resistance and beta cell dysfunction induced by a high-fat diet. Diabetologia. 2010;53(8):1795–806.

    Article  CAS  PubMed  Google Scholar 

  36. Hirabara SM, Curi R, Maechler P. Saturated fatty acid-induced insulin resistance is associated with mitochondrial dysfunction in skeletal muscle cells. J Cell Physiol. 2010;222(1):187–94.

    Article  CAS  PubMed  Google Scholar 

  37. Jové M, Planavila A, Laguna JC, et al. Palmitate-induced interleukin 6 production is mediated by protein kinase C and nuclear-factor κB activation and leads to glucose transporter 4 down-regulation in skeletal muscle cells. Endocrinology. 2005;146(7):3087–95.

    Article  PubMed  Google Scholar 

  38. Tiganis T. Reactive oxygen species and insulin resistance: the good, the bad and the ugly. Trends Pharmacol Sci. 2011;32(2):82–9.

    Article  CAS  PubMed  Google Scholar 

  39. Ma W, Wu JH, Wang Q, et al. Prospective association of fatty acids in the de novo lipogenesis pathway with risk of type 2 diabetes: the Cardiovascular Health Study. Am J Clin Nutr. 2015;101(1):153–63.

    Article  CAS  PubMed  Google Scholar 

  40. Shah M, Adams-Huet B, Brinkley L, et al. Lipid, glycemic, and insulin responses to meals rich in saturated, cis-monounsaturated, and polyunsaturated (n-3 and n-6) fatty acids in subjects with type 2 diabetes. Diabetes Care. 2007;30(12):2993–8.

    Article  CAS  PubMed  Google Scholar 

  41. Grapov D, Adams SH, Pedersen TL, et al. Type 2 diabetes associated changes in the plasma non-esterified fatty acids, oxylipins and endocannabinoids. PLoS One. 2012;7(11):e48852.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  42. Imamura S, Morioka T, Yamazaki Y, et al. Plasma polyunsaturated fatty acid profile and delta-5 desaturase activity are altered in patients with type 2 diabetes. Metabolism. 2014;63(11):1432–8.

    Article  CAS  PubMed  Google Scholar 

  43. Griffo E, Nosso G, Lupoli R, et al. Early improvement of postprandial lipemia after bariatric surgery in obese type 2 diabetic patients. Obes Surg. 2014;24(5):765–70.

    Article  CAS  PubMed  Google Scholar 

  44. Jørgensen NB, Dirksen C, Bojsen-Møller KN, et al. Exaggerated glucagon-like peptide 1 response is important for improved β-cell function and glucose tolerance after Roux-en-Y gastric bypass in patients with type 2 diabetes. Diabetes. 2013;62(9):3044–52.

    Article  PubMed  PubMed Central  Google Scholar 

  45. Rocca A, Brubaker P. Role of the vagus nerve in mediating proximal nutrient-induced glucagon-like peptide-1 secretion 1. Endocrinology. 1999;140(4):1687–94.

    CAS  PubMed  Google Scholar 

  46. Nauck MA. Unraveling the science of incretin biology. Am J Med. 2009;122(6):S3–S10.

    Article  PubMed  Google Scholar 

  47. Isbell JM, Tamboli RA, Hansen EN, et al. The importance of caloric restriction in the early improvements in insulin sensitivity after Roux-en-Y gastric bypass surgery. Diabetes Care. 2010;33(7):1438–42.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  48. Burcelin R, Serino M, Cabou C. A role for the gut-to-brain GLP-1-dependent axis in the control of metabolism. Curr Opin Pharmacol. 2009;9(6):744–52.

    Article  CAS  PubMed  Google Scholar 

  49. Hirasawa A, Tsumaya K, Awaji T, et al. Free fatty acids regulate gut incretin glucagon-like peptide-1 secretion through GPR120. Nat Med. 2005;11(1):90–4.

    Article  CAS  PubMed  Google Scholar 

  50. DeFronzo RA, Tobin JD, Andres R. Glucose clamp technique: a method for quantifying insulin secretion and resistance. American Journal of Physiology-Gastrointestinal and Liver Physiology. 1979;237(3):G214–G23.

    Google Scholar 

Download references

Acknowledgments

This study was supported by Jens Henrik Jensen Academic Fellowship and Auckland A+ Research Trust.

Author information

Authors and Affiliations

  1. School of Applied Sciences, Faculty of Health and Environmental Sciences, Auckland University of Technology, Auckland, New Zealand

    Reza Nemati & Jun Lu

  2. School of Interprofessional Health Studies, Faculty of Health and Environmental Sciences, Auckland University of Technology, Auckland, New Zealand

    Jun Lu

  3. Institute of Biomedical Technology, Auckland University of Technology, Auckland, New Zealand

    Jun Lu

  4. Metabolic Unit, Institute of Neuroscience, National Research Council, 35127, Padua, Italy

    Andrea Tura

  5. Department of Pharmacology, University of New South Wales, Sydney, Australia

    Greg Smith

  6. Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, Private Bag 92019, Auckland, 1142, New Zealand

    Rinki Murphy

Authors
  1. Reza Nemati
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Jun Lu
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Andrea Tura
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Greg Smith
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Rinki Murphy
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Rinki Murphy.

Ethics declarations

This study was approved by the local ethics committee (Northern X Regional ethics committee), and all patients gave informed written consent.

Conflict of Interest

The authors declare that they have no conflict of interest.

A Statement of Informed Consent

Informed consent was obtained from all individual participants included in the study.

Financial Support

We acknowledge financial support from the Faculty of Health and Environmental Sciences, Auckland University of Technology, and from Lottery Health Research and Maurice and Phyllis Paykel Trust for the LC-MS facility.

Electronic supplementary material

ESM 1

(DOCX 17.8 kb)

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Nemati, R., Lu, J., Tura, A. et al. Acute Changes in Non-esterified Fatty Acids in Patients with Type 2 Diabetes Receiving Bariatric Surgery. OBES SURG 27, 649–656 (2017). https://doi.org/10.1007/s11695-016-2323-9

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s11695-016-2323-9

Keywords

Search

Navigation