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Cell Metab. 2018 Oct 2;28(4):547-556.e3. doi: 10.1016/j.cmet.2018.07.003. Epub 2018 Aug 2.

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

Author information

1
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.
2
Newcastle Magnetic Resonance Centre, Institute of Cellular Medicine, Newcastle University, Campus for Ageing & Vitality, Newcastle upon Tyne NE4 5PL, UK.
3
Human Nutrition Research Centre, Institute of Health & Society, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
4
Department of Computer Science, Lagos State University, Ojo, Lagos State, Nigeria.
5
Human Nutrition Research Centre, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
6
Institute of Cardiovascular and Medical Science, University of Glasgow, Glasgow G12 8TA, UK.
7
Human Nutrition, School of Medicine, Dentistry and Nursing, College of Medical, Veterinary & Life Sciences, University of Glasgow, Glasgow G31 2ER, UK.

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.

KEYWORDS:

human; insulin secretion; liver fat; low-calorie diet; pancreas fat; type 2 diabetes; type 2 diabetes remission; very low-density lipoprotein; weight loss; β cell dedifferentiation

PMID:
30078554
DOI:
10.1016/j.cmet.2018.07.003
[Indexed for MEDLINE]
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