Abstract
Although lifestyle interventions can lead to diabetes remission, it is unclear to what extent type 2 diabetes (T2D) remission alters or improves the underlying pathophysiology of the disease. Here, we assess the effects of a lifestyle intervention on T2D reversal or remission and the effects on the underlying pathology. In a Dutch primary care setting, 15 adults with an average T2D duration of 13.4 years who were (pharmacologically) treated for T2D received a diabetes subtyping (“diabetyping”) lifestyle intervention (DLI) for six months, aiming for T2D remission. T2D subtype was determined based on an OGTT. Insulin and sulphonylurea (SU) derivative treatment could be terminated for all participants. Body weight, waist/hip ratio, triglyceride levels, HbA1c, fasting, and 2h glucose were significantly improved after three and six months of intervention. Remission and reversal were achieved in two and three participants, respectively. Indices of insulin resistance and beta cell capacity improved, but never reached healthy values, resulting in unchanged T2D subtypes. Our study implies that achieving diabetes remission in individuals with a longer T2D duration is possible, but underlying pathology is only minimally affected, possibly due to an impaired beta cell function. Thus, even when T2D remission is achieved, patients need to continue adhering to lifestyle therapy.
Highlights
Type 2 diabetes (T2D) has become a global health burden [1]
We propose the Diabetyping Lifestyle Intervention (DLI), in which the oral glucose tolerance test (OGTT) is used to determine the diabetic subtype in individuals with T2D
Years diagnosed with T2D Body height (m) Body weight body mass index (BMI)
Summary
T2D refers to a metabolic glucose dysregulation resulting from insulin resistance (IR) and inadequate insulin secretion [2], the etiology of T2D is highly heterogeneous [3]. T2D is preceded by insulin resistance, and ensues when the pancreas becomes unable to compensate for insulin resistance, resulting in glucose intolerance and hyperglycemia [4]. Prolonged hyperglycemia can induce glucotoxicity, which causes beta cell dysfunction and altered beta cell mass, contributing to further deterioration of T2D [5]. The primary pathophysiological defects in T2D are IR of the liver, muscle, and/or adipose tissue, as well as impaired pancreatic beta cell function (BCF) [6]. The severity of IR in insulin-sensitive cells is not uniform, and may differ among various tissues [7,8]. The development of T2D results from the interaction of a person’s genetic makeup with their environment [9], with risk factors being obesity, unhealthy diet and physical inactivity [10]
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