Journal
DIABETES OBESITY & METABOLISM
Volume 21, Issue 8, Pages 1861-1870Publisher
WILEY
DOI: 10.1111/dom.13744
Keywords
apolipoprotein C-III; kinetics; lipoproteins; stable isotopes; type 2 diabetes
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Funding
- IIS grants from NovoNordisk
- Swedish Heart-Lung Foundation
- Swedish Diabetes Foundation
- Swedish Research Council
- Swedish Foundation for Strategic Research
- Helsinki University Hospital Research funds
- EU project RESOLVE
- Finnish Heart Foundation
- Academy of Finland [314383, 272376, 266286]
- Finnish Medical Foundation
- Finnish Diabetes Research Foundation
- Novo Nordisk Foundation
- Gyllenberg Foundation
- Sahlgrenska University Hospital
- Sigrid Juselius Foundation
- Academy of Finland (AKA) [314383, 266286, 266286, 314383] Funding Source: Academy of Finland (AKA)
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Aims To investigate how apolipoprotein C-III (apoC-III) metabolism is altered in subjects with type 2 diabetes, whether the perturbed plasma triglyceride concentrations in this condition are determined primarily by the secretion rate or the removal rate of apoC-III, and whether improvement of glycaemic control using the glucagon-like peptide-1 analogue liraglutide for 16 weeks modifies apoC-III dynamics. Materials and Methods Postprandial apoC-III kinetics were assessed after a bolus injection of [5,5,5-H-2(3)]leucine using ultrasensitive mass spectrometry techniques. We compared apoC-III kinetics in two situations: in subjects with type 2 diabetes before and after liraglutide therapy, and in type 2 diabetic subjects with matched body mass index (BMI) non-diabetic subjects. Liver fat content, subcutaneous abdominal and intra-abdominal fat were determined using proton magnetic resonance spectroscopy. Results Improved glycaemic control by liraglutide therapy for 16 weeks significantly reduced apoC-III secretion rate (561 +/- 198 vs. 652 +/- 196 mg/d, P = 0.03) and apoC-III levels (10.0 +/- 3.8 vs. 11.7 +/- 4.3 mg/dL, P = 0.035) in subjects with type 2 diabetes. Change in apoC-III secretion rate was significantly associated with the improvement in indices of glucose control (r = 0.67; P = 0.009) and change in triglyceride area under the curve (r = 0.59; P = 0.025). In line with this, the apoC-III secretion rate was higher in subjects with type 2 diabetes compared with BMI-matched non-diabetic subjects (676 +/- 208 vs. 505 +/- 174 mg/d, P = 0.042). Conclusions The results reveal that the secretion rate of apoC-III is associated with elevation of triglyceride-rich lipoproteins in subjects with type 2 diabetes, potentially through the influence of glucose homeostasis on the production of apoC-III.
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