Assessment of Basal Insulin Requirement Using Fasting Tests in Insulin-treated Patients with Type 2 Diabetes Mellitus

 

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Abstract

Aims: Characterizing the time course of the rise of blood glucose concentrations in the fasting state during the day and night in patients with type 2 diabetes. Methods: 40 consecutive insulin-treated patients with type 2 diabetes underwent fasting tests on two different days with either no breakfast and lunch (fasting time of 20 hours) or no dinner (fasting time of 21 hours). Glucose-lowering medication was stopped prior to the test according to the half-life of the medication prescribed. At the start of the fasting tests, blood glucose concentrations were lowered to below 7 mmol/L using an insulin infusion. Results: 26 men and 14 women were included in the study. Mean (±SD) age was 61±10 years, BMI 31±7 kg/m², and HbA1c 7.5±1%. Diabetes duration was 14±8 years and duration of insulin therapy had been prescribed for a mean of 6±6 years. During the daytime fast, plasma glucose concentrations rose by a mean of 0.8±1.6 mmol/L. During the nighttime fast, plasma glucose concentrations increased particularly after midnight, by 4.3±2.1 mmol/L, i.e. significantly more than during the daytime fast. Conclusions: Fasting blood glucose concentrations in the majority of insulin-treated patients with type 2 diabetes increase markedly after midnight. No similar increase is observed during the day. Thus, for most patients with type 2 diabetes, an intermediate- or long-acting insulin injected at bedtime with a peak action six to eight hours after injection should be appropriate.

References

• 1 Bolli GB, Owens DR. Insulin glargine.  Lancet. 2000;  356 443-445
  CrossrefPubMedGoogle Scholar
• 2 Bray GA. Risks of obesity.  Endocrinol Metab Clin North Am. 2003;  32 787-804
  CrossrefPubMedGoogle Scholar
• 3 Burge MR, Schade DS. Insulins.  Endocrinol Metab Clin North Am. 1997;  26 575-598
  CrossrefPubMedGoogle Scholar
• 4 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
  CrossrefPubMedGoogle Scholar
• 5 DeWitt DE, Hirsch IB. Outpatient insulin therapy in type 1 and type 2 diabetes mellitus: scientific review.  Jama. 2003;  289 2254-2264
  PubMedGoogle Scholar
• 6 Goodpaster BH, Krishnaswami S, Resnick H, Kelley DE, Haggerty C, Harris TB, Schwartz AV, Kritchevsky S, Newman AB. Association between regional adipose tissue distribution and both type 2 diabetes and impaired glucose tolerance in elderly men and women.  Diabetes Care. 2003;  26 372-379
  CrossrefPubMedGoogle Scholar
• 7 Haupt E, Haupt A, Herrmann R, Benecke-Timp A, Vogel H, Walter C. The KID Study V: the natural history of type 2 diabetes in younger patients still practising a profession. Heterogeneity of basal and reactive C-peptide levels in relation to BMI, duration of disease, age and HbA1.  Exp Clin Endocrinol Diabetes. 1999;  107 236-243
  PubMedGoogle Scholar
• 8 Heise T, Nosek L, Ronn BB, Endahl L, Heinemann L, Kapitza C, Draeger E. Lower within-subject variability of insulin detemir in comparison to NPH insulin and insulin glargine in people with type 1 diabetes.  Diabetes. 2004;  53 1614-1620
  CrossrefPubMedGoogle Scholar
• 9 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
  CrossrefPubMedGoogle Scholar
• 10 Kahn SE. The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes.  Diabetologia. 2003;  46 3-19
  CrossrefPubMedGoogle Scholar
• 11 Lepore M, Pampanelli S, Fanelli C, Porcellati F, Bartocci L, Di Vincenzo A, Cordoni C, Costa E, Brunetti P, Bolli GB. Pharmacokinetics and pharmacodynamics of subcutaneous injection of long-acting human insulin analog glargine, NPH insulin, and ultralente human insulin and continuous subcutaneous infusion of insulin lispro.  Diabetes. 2000;  49 2142-2148
  CrossrefPubMedGoogle Scholar
• 12 Mitrakou A, Kelley D, Mokan M, Veneman T, Pangburn T, Reilly J, Gerich J. Role of reduced suppression of glucose production and diminished early insulin release in impaired glucose tolerance.  N Engl J Med. 1992;  326 22-29
  PubMedGoogle Scholar
• 13 Mudaliar S, Edelman SV. Insulin therapy in type 2 diabetes.  Endocrinol Metab Clin North Am. 2001;  30 935-982
  PubMedGoogle Scholar
• 14 Waldhausl WK. The physiological basis of insulin treatment-clinical aspects.  Diabetologia. 1986;  29 837-849
  CrossrefPubMedGoogle Scholar
• 15 Wiesli P, Schaffler E, Seifert B, Schmid C, Donath MY. Islets secretory capacity determines glucose homoeostasis in the face of insulin resistance.  Swiss Med Wkly. 2004;  134 559-564
  PubMedGoogle Scholar

Correspondence

Peter WiesliMD 

Division of Endocrinology and Diabetes

Kantonsspital Frauenfeld

·CH-8500 Frauenfeld

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