UK Prospective Diabetes Study V. Characteristics of Newly presenting Type 2 Diabetic Patients: Estimated Insulin Sensitivity and Islet B‐cell Function

Abstract

In 713 newly diagnosed Caucasian diabetic patients aged 25–65 inclusive, insulin sensitivity and islet B‐cell function were estimated from fasting plasma glucose and insulin concentrations by Homeostasis Model Assessment. Insulin sensitivity was reduced in obese subjects. It was also slightly lower in male than in female diabetic patients, in those who were sedentary and in those with high fasting plasma glucose concentrations. The estimated B‐cell function was particularly impaired in patients with a high fasting plasma glucose and in those with normal rather than excess body weight. Whilst diabetes can present in normal weight patients with marked deficiency of B‐cell function, presenting patients often have only a moderate impairment of B‐cell function with markedly impaired insulin sensitivity secondary to obesity, physical inactivity, or being male.

Diabetes Remission after Nonsurgical Intensive Lifestyle Intervention in Obese Patients with Type 2 Diabetes

“…The concept of diabetes remission in established patients who are already treated with antihyperglycemic medications is intriguing as it contradicts the traditional concept that type 2 diabetes is a chronic progressive disease characterized by significant loss of beta-cell function (up to 80%) at the time of diagnosis [16, 17]. Bergman et al originally challenged this concept in obese patients with type 2 diabetes although he confirmed its existence in lean patients.…”

“…It is worth mentioning that the United Kingdom Prospective Diabetes Study (UKPDS), which created that concept, was not originally designed to evaluate beta-cell function [21]. The study used a rough technique (HOMA calculation) to retrospectively calculate beta-cell function and create a hypothetical graph that indicates a progressive decline of beta-cell function [17]. The impossibility of acquiring pancreatic biopsies from living individuals with type 2 diabetes limits our knowledge about the actual beta-cell volume and function in living humans.…”