Remission of Human Type 2 Diabetes Requires Decrease in Liver and Pancreas Fat Content but Is Dependent upon Capacity for β Cell Recovery.

Newcastle Magnetic Resonance Centre, Institute of Cellular Medicine, Newcastle University, Campus for Ageing & Vitality, Newcastle upon Tyne NE4 5PL, UK. Electronic address: roy.taylor@ncl.ac.uk. Newcastle Magnetic Resonance Centre, Institute of Cellular Medicine, Newcastle University, Campus for Ageing & Vitality, Newcastle upon Tyne NE4 5PL, UK. Human Nutrition Research Centre, Institute of Health & Society, Newcastle University, Newcastle upon Tyne NE2 4HH, UK. Department of Computer Science, Lagos State University, Ojo, Lagos State, Nigeria. Human Nutrition Research Centre, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK. Institute of Cardiovascular and Medical Science, University of Glasgow, Glasgow G12 8TA, UK. Human Nutrition, School of Medicine, Dentistry and Nursing, College of Medical, Veterinary & Life Sciences, University of Glasgow, Glasgow G31 2ER, UK.

Cell metabolism. 2018;(4):547-556.e3
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Abstract

The Diabetes Remission Clinical Trial reported return and persistence of non-diabetic blood glucose control in 46% of people with type 2 diabetes of up to 6 years duration. Detailed metabolic studies were performed on a subgroup (intervention, n = 64; control, n = 26). In the intervention group, liver fat content decreased (16.0% ± 1.3% to 3.1% ± 0.5%, p < 0.0001) immediately after weight loss. Similarly, plasma triglyceride and pancreas fat content decreased whether or not glucose control normalized. Recovery of first-phase insulin response (0.04[-0.05-0.32] to 0.11[0.0005-0.51] nmol/min/m2, p < 0.0001) defined those who returned to non-diabetic glucose control and this was durable at 12 months (0.11[0.005-0.81] nmol/min/m2, p = 0.0001). Responders were similar to non-responders at baseline but had shorter diabetes duration (2.7 ± 0.3 versus 3.8 ± 0.4 years; p = 0.02). This study demonstrates that β cell ability to recover long-term function persists after diagnosis, changing the previous paradigm of irreversible loss of β cell function in type 2 diabetes.

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