Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Clinical Trial
. 2011 Oct;54(10):2506-14.
doi: 10.1007/s00125-011-2204-7. Epub 2011 Jun 9.

Reversal of Type 2 Diabetes: Normalisation of Beta Cell Function in Association With Decreased Pancreas and Liver Triacylglycerol

Affiliations
Free PMC article
Clinical Trial

Reversal of Type 2 Diabetes: Normalisation of Beta Cell Function in Association With Decreased Pancreas and Liver Triacylglycerol

E L Lim et al. Diabetologia. .
Free PMC article

Abstract

Aims/hypothesis: Type 2 diabetes is regarded as inevitably progressive, with irreversible beta cell failure. The hypothesis was tested that both beta cell failure and insulin resistance can be reversed by dietary restriction of energy intake.

Methods: Eleven people with type 2 diabetes (49.5 ± 2.5 years, BMI 33.6 ± 1.2 kg/m(2), nine male and two female) were studied before and after 1, 4 and 8 weeks of a 2.5 MJ (600 kcal)/day diet. Basal hepatic glucose output, hepatic and peripheral insulin sensitivity and beta cell function were measured. Pancreas and liver triacylglycerol content was measured using three-point Dixon magnetic resonance imaging. An age-, sex- and weight-matched group of eight non-diabetic participants was studied.

Results: After 1 week of restricted energy intake, fasting plasma glucose normalised in the diabetic group (from 9.2 ± 0.4 to 5.9 ± 0.4 mmol/l; p = 0.003). Insulin suppression of hepatic glucose output improved from 43 ± 4% to 74 ± 5% (p = 0.003 vs baseline; controls 68 ± 5%). Hepatic triacylglycerol content fell from 12.8 ± 2.4% in the diabetic group to 2.9 ± 0.2% by week 8 (p = 0.003). The first-phase insulin response increased during the study period (0.19 ± 0.02 to 0.46 ± 0.07 nmol min(-1) m(-2); p < 0.001) and approached control values (0.62 ± 0.15 nmol min(-1) m(-2); p = 0.42). Maximal insulin response became supranormal at 8 weeks (1.37 ± 0.27 vs controls 1.15 ± 0.18 nmol min(-1) m(-2)). Pancreatic triacylglycerol decreased from 8.0 ± 1.6% to 6.2 ± 1.1% (p = 0.03).

Conclusions/interpretation: Normalisation of both beta cell function and hepatic insulin sensitivity in type 2 diabetes was achieved by dietary energy restriction alone. This was associated with decreased pancreatic and liver triacylglycerol stores. The abnormalities underlying type 2 diabetes are reversible by reducing dietary energy intake.

Figures

Fig. 1
Fig. 1
Effect of 8 weeks of dietary intervention on (a) plasma glucose, (b) hepatic glucose production (HGP) and (c) hepatic triacylglycerol content (TG) for diabetic participants (black triangles). White circles indicate the mean for the weight-matched non-diabetic control group. Data are shown as mean ± SE
Fig. 2
Fig. 2
Insulin secretion test data in controls and in diabetic participants at each time point. a Plasma glucose levels achieved in each group. Insulin section rate (ISR) obtained in (b) the non-diabetic control group, (c) the diabetic group at baseline, (d) the diabetic group at 1 week of the diet, (e) the diabetic group at 4 weeks and (f) the diabetic group at 8 weeks. Data are shown as mean ± SE
Fig. 3
Fig. 3
a Change in first-phase insulin response, and (b) change in pancreas triacylglycerol (TG) content during the 8 week dietary intervention in diabetic individuals (black triangles). White circles indicate the mean for the weight-matched non-diabetic control group. Data are shown as mean ± SE

Comment in

  • Type 2 diabetes: remission in just a week.
    Yki-Järvinen H. Yki-Järvinen H. Diabetologia. 2011 Oct;54(10):2477-9. doi: 10.1007/s00125-011-2266-6. Epub 2011 Aug 9. Diabetologia. 2011. PMID: 21826485 No abstract available.

Similar articles

See all similar articles

Cited by 222 articles

See all "Cited by" articles

References

    1. UK Prospective Diabetes Study Group Intensive blood glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33) Lancet. 1999;352:837–853. - PubMed
    1. Prospective Diabetes Study Group UK. Overview of 6 years' therapy of type II diabetes: a progressive disease. UK Prospective Diabetes Study 16. Diabetes. 1995;44:1249–1258. doi: 10.2337/diabetes.44.11.1249. - DOI - PubMed
    1. Weyer C, Bogardus C, Mott DM, Pratley RE. The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus. J Clin Invest. 1999;104:787–794. doi: 10.1172/JCI7231. - DOI - PMC - PubMed
    1. Kahn SE. The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes. Diabetologia. 2003;46:3–19. doi: 10.1007/s00125-003-1190-9. - DOI - PubMed
    1. Butler AE, Janson J, Bonner-Weir S, Ritzel R, Rizza RA, Butler PC. Beta-cell deficit and increased beta-cell apoptosis in humans with type 2 diabetes. Diabetes. 2003;52:102–110. doi: 10.2337/diabetes.52.1.102. - DOI - PubMed

Publication types

Feedback