Assessment of endogenous insulin secretion in insulin treated diabetes predicts postprandial glucose and treatment response to prandial insulin

BMC Endocrine Disorders

Andrew T Hattersley¹  Bridget A Knight¹  Suzy V Hope¹  Timothy J McDonald²  Beverley M Shields¹  Rachel EJ Besser¹  Angus G Jones¹ 

[1] Peninsula NIHR Clinical Research Facility, Peninsula Medical School, University of Exeter, Exeter, UK;Royal Devon and Exeter Hospital, Barrack Road, Exeter, EX2 5DW, UK

关键词: Insulin;    Glucose;    Postprandial;    C-peptide;    Diabetes;   

Others  :  1086431
DOI  :  10.1186/1472-6823-12-6

 received in 2012-01-10, accepted in 2012-06-08,  发布年份 2012

【 摘 要 】

Background

In patients with both Type 1 and Type 2 diabetes endogenous insulin secretion falls with time which changes treatment requirements, however direct measurement of endogenous insulin secretion is rarely performed. We aimed to assess the impact of endogenous insulin secretion on postprandial glucose increase and the effectiveness of prandial exogenous insulin.

Methods

We assessed endogenous insulin secretion in 102 participants with insulin treated diabetes (58 Type 1) following a standardised mixed meal without exogenous insulin. We tested the relationship between endogenous insulin secretion and post meal hyperglycaemia. In 80 participants treated with fast acting breakfast insulin we repeated the mixed meal with participants’ usual insulin given and assessed the impact of endogenous insulin secretion on response to exogenous prandial insulin.

Results

Post meal glucose increment (90 minute - fasting) was inversely correlated with endogenous insulin secretion (90 minute C-peptide) (Spearman’s r = −0.70, p < 0.001). Similar doses of exogenous prandial insulin lowered glucose increment more when patients had less endogenous insulin; by 6.4(4.2-11.1) verses 1.2(0.03-2.88) mmol/L (p < 0.001) for patients in the lowest verses highest tertiles of endogenous insulin.

Conclusions

In insulin treated patients the measurement of endogenous insulin secretion may help predict the degree of postprandial hyperglycaemia and the likely response to prandial insulin.

【 授权许可】

   
2012 Jones et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

Figure 2.

【 参考文献 】

• [1]National Institute of Clinical Excellence (UK): Guideline CG87 - Type 2 diabetes: the management of type 2 diabetes. 2009.
• [2]National Institute of Clinical Excellence (UK): Guideline CG15, Type 1 diabetes in adults. 2004.
• [3]DeWitt DE, Hirsch IB: Outpatient insulin therapy in type 1 and type 2 diabetes mellitus: scientific review. JAMA 2003, 289:2254-2264.
• [4]The Diabetes Control and Complications Trial Research Group: Effect of intensive therapy on residual beta-cell function in patients with type 1 diabetes in the diabetes control and complications trial. A randomized, controlled trial. Ann Intern Med 1998, 128:517-523.
• [5]Kahn SE: Clinical review 135: The importance of beta-cell failure in the development and progression of type 2 diabetes. J Clin Endocrinol Metab 2001, 86:4047-4058.
• [6]Turner RC, Cull CA, Frighi V, Holman RR: Glycemic control with diet, sulfonylurea, metformin, or insulin in patients with type 2 diabetes mellitus: progressive requirement for multiple therapies (UKPDS 49). UK Prospective Diabetes Study (UKPDS) Group. JAMA 1999, 281:2005-2012.
• [7]Hoekstra JB, Van Rijn HJ, Thijssen JH, Erkelens DW: C-peptide reactivity as a measure of insulin dependency in obese diabetic patients treated with insulin. Diabetes Care 1982, 5:585-591.
• [8]Hohberg C, Pfutzner A, Forst T, Lubben G, Karagiannis E, Borchert M, Schondorf T: Successful switch from insulin therapy to treatment with pioglitazone in type 2 diabetes patients with residual beta-cell function: results from the PioSwitch study. Diabetes Obes Metab 2009, 11:464-471.
• [9]Hermann LS, Schersten B, Melander A: Antihyperglycaemic efficacy, response prediction and dose–response relations of treatment with metformin and sulphonylurea, alone and in primary combination. Diabet Med 1994, 11:953-960.
• [10]Lee A, Morley J: Classification of type 2 diabetes by clinical response to metformin-troglitazone combination and C-Peptide criteria. Endocr Pract 1999, 5:305-313.
• [11]Grant PJ, Barlow E, Miles DW: Plasma C-peptide levels identify insulin-treated diabetic patients suitable for oral hypoglycaemic therapy. Diabet Med 1984, 1:284-286.
• [12]Madsbad S, Krarup T, McNair P, Christiansen C, Faber OK, Transbol I, Binder C: Practical clinical value of the C-peptide response to glucagon stimulation in the choice of treatment in diabetes mellitus. Acta Med Scand 1981, 210:153-156.
• [13]Munshi MN, Hayes M, Sternthal A, Ayres D: Use of serum c-peptide level to simplify diabetes treatment regimens in older adults. Am J Med 2009, 122:395-397.
• [14]Laakso M, Sarlund H, Korhonen T, Voutilainen E, Majander H, Hakala P, Uusitupa M, Pyorala K: Stopping insulin treatment in middle-aged diabetic patients with high postglucagon plasma C-peptide. Effect on glycaemic control, serum lipids and lipoproteins. Acta Med Scand 1988, 223:61-68.
• [15]Blaum CS, Velez L, Hiss RG, Halter JB: Characteristics related to poor glycemic control in NIDDM patients in community practice. Diabetes Care 1997, 20:7-11.
• [16]Chan WB, Chan JC, Chow CC, Yeung VT, So WY, Li JK, Ko GT, Ma RC, Cockram CS: Glycaemic control in type 2 diabetes: the impact of body weight, beta-cell function and patient education. QJM 2000, 93:183-190.
• [17]Koskinen P, Viikari J, Irjala K, Kaihola HL, Seppala P: Plasma and urinary C-peptide in the classification of adult diabetics. Scand J Clin Lab Invest 1986, 46:655-663.
• [18]Hother-Nielsen O, Faber O, Sorensen NS, Beck-Nielsen H: Classification of newly diagnosed diabetic patients as insulin-requiring or non-insulin-requiring based on clinical and biochemical variables. Diabetes Care 1988, 11:531-537.
• [19]Saisho Y, Kou K, Tanaka K, Abe T, Kurosawa H, Shimada A, Meguro S, Kawai T, Itoh H: Postprandial serum C-peptide to plasma glucose ratio as a predictor of subsequent insulin treatment in patients with type 2 diabetes. Endocr J 2011, 58:315-322.
• [20]Clark PM: Assays for insulin, proinsulin(s) and C-peptide. Ann Clin Biochem 1999, 36(Pt 5):541-564.
• [21]Greenbaum CJ, Mandrup-Poulsen T, McGee PF, Battelino T, Haastert B, Ludvigsson J, Pozzilli P, Lachin JM, Kolb H: Mixed-meal tolerance test versus glucagon stimulation test for the assessment of beta-cell function in therapeutic trials in type 1 diabetes. Diabetes Care 2008, 31:1966-1971.
• [22]Yki-Jarvinen H: Combination therapies with insulin in type 2 diabetes. Diabetes Care 2001, 24:758-767.
• [23]Holman RR, Farmer AJ, Davies MJ, Levy JC, Darbyshire JL, Keenan JF, Paul SK: Three-year efficacy of complex insulin regimens in type 2 diabetes. N Engl J Med 2009, 361:1736-1747.
• [24]Jones AG, Besser REJ, McDonald TJ, Shields BM, Hope SV, Bowman P, Oram RA, Knight BA, Hattersley AT: Urine C-peptide creatinine ratio (UCPCR) is an alternative to stimulated serum C-peptide measurement in late onset insulin treated diabetes. Diabet Med 2011, 28(9):1034-1038.
• [25]Besser RE, Ludvigsson J, Jones AG, McDonald TJ, Shields BM, Knight BA, Hattersley AT: Urine C-peptide creatinine ratio is a noninvasive alternative to the mixed-meal tolerance test in children and adults with type 1 diabetes. Diabetes Care 2011, 34(3):607-609.
• [26]McDonald TJ, Knight BA, Shields BM, Bowman P, Salzmann MB, Hattersley AT: Stability and reproducibility of a single-sample urinary C-Peptide/Creatinine ratio and its correlation with 24-h Urinary C-Peptide. Clin Chem 2009, 55(11):2035-2039.
• [27]Ferrannini E, Gastaldelli A, Miyazaki Y, Matsuda M, Mari A, DeFronzo RA: Beta-Cell function in subjects spanning the range from normal glucose tolerance to overt diabetes: a new analysis. J Clin Endocrinol Metab 2005, 90:493-500.
• [28]Kohnert KD, Augstein P, Zander E, Heinke P, Peterson K, Freyse EJ, Hovorka R, Salzsieder E: Glycemic variability correlates strongly with postprandial beta-cell dysfunction in a segment of type 2 diabetic patients using oral hypoglycemic agents. Diabetes Care 2009, 32:1058-1062.
• [29]Shapiro AM, Ricordi C, Hering BJ, Auchincloss H, Lindblad R, Robertson RP, Secchi A, Brendel MD, Berney T, Brennan DC, et al.: International trial of the Edmonton protocol for islet transplantation. N Engl J Med 2006, 355:1318-1330.
• [30]Naik RG, Brooks-Worrell BM, Palmer JP: Latent autoimmune diabetes in adults. J Clin Endocrinol Metab 2009, 94:4635-4644.
• [31]Fonseca VA: Defining and characterizing the progression of type 2 diabetes. Diabetes Care 2009, 32(Suppl 2):S151-S156.
• [32]Swinnen SG, Hoekstra JB, DeVries JH: Insulin therapy for type 2 diabetes. Diabetes Care 2009, 32(Suppl 2):S253-S259.