Abstract
Autoimmune destruction of pancreatic β-cells results in the permanent loss of insulin production in type 1 diabetes (T1D). The daily necessity to inject exogenous insulin to treat hyperglycemia leads to a relative portal vein insulin deficiency and potentiates hypoglycemia which can induce weight gain, while daily fluctuations of blood sugar levels affect the hepatic glycogen storage and overall metabolic control. These, among others, fundamental characteristics of T1D are associated with the development of two distinct, but in part clinically similar hepatopathies, namely non-alcoholic fatty liver disease (NAFLD) and glycogen hepatopathy (GlyH). Recent studies suggest that NAFLD may be increasingly common in T1D because more people with T1D present with overweight and/or obesity, linked to the metabolic syndrome. GlyH is a rare but underdiagnosed complication hallmarked by extremely brittle metabolic control in, often young, individuals with T1D. Both hepatopathies share clinical similarities, troubling both diagnosis and differentiation. Since NAFLD is increasingly associated with cardiovascular and chronic kidney disease, whereas GlyH is considered self-limiting, awareness and differentiation between both condition is important in clinical care. The exact pathogenesis of both hepatopathies remains obscure, hence licensed pharmaceutical therapy is lacking and general awareness amongst physicians is low. This article aims to review the factors potentially contributing to fatty liver disease or glycogen storage disruption in T1D. It ends with a proposal for clinicians to approach patients with T1D and potential hepatopathy.
Highlights
Type 1 diabetes mellitus (T1D) is caused by autoimmune destruction of the insulin-producing pancreatic β-cells resulting in chronic hyperglycemia and lifelong exogenous insulin dependency (American Diabetes Association, 2021a)
This study reported that the prevalence of steatosis was 12.6% based on classical ultrasound and 16.8% based on controlled attenuation parameter (CAP), a novel ultrasound-based marker of steatosis available on the Fibroscan© device (Echosens, Paris, France)
T1D patients are not protected from the effects of overweight and/ or insulin resistance
Summary
Type 1 diabetes mellitus (T1D) is caused by autoimmune destruction of the insulin-producing pancreatic β-cells resulting in chronic hyperglycemia and lifelong exogenous insulin dependency (American Diabetes Association, 2021a). Already in 1975, Baum et al described that increased weight gain in infancy could be linked to the development of T1D (Baum et al, 1975; Lauria et al, 2015). This hypothesis is further fueled by an increased odds ratio to develop T1D when childhood adiposity was present (Censin et al, 2017), and a lower risk of T1D associated with the presence of an insulin sensitivity-increasing polymorphism (Raj et al, 2009). Since the global incidence of both (childhood) obesity (Blüher, 2019; Di Cesare et al, 2019) and T1D are rising (Mobasseri et al, 2020), there might be a common pathway leading to increased β-cell fragility and subsequent development of diabetes, in the presence of other stressors, leading to patients with both T1D and an already present chronic metabolic dysfunction (Liston et al, 2017)
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