Publications by authors named "Markku T Taittonen"

3 Publications

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Myocardial glucose uptake in patients with the m.3243A > G mutation in mitochondrial DNA.

J Inherit Metab Dis 2016 Jan 26;39(1):67-74. Epub 2015 Jun 26.

Research Group of Clinical Neuroscience, Neurology, University of Oulu, P.O Box 5000, FIN-90014, Oulu, Finland.

Mitochondrial mutations impair glucose oxidation and increase glucose uptake in cell cultures and lead to cardiomyopathy in patients. Here we characterize cardiac glucose uptake in 14 patients with the m.3243A > G mutation in mitochondrial DNA. The 14 patients with m.3243A > G and 13 controls were similar in age, physical activity and body mass index. Ten patients had diabetes. Left ventricular glucose uptake per tissue mass (LVGU) was measured with 2-[(18) F]fluoro-2-deoxyglucose positron emission tomography during euglycemic hyperinsulinemia. Cardiac morphology and function were assessed with magnetic resonance imaging. We found that the LVGU was 25% lower in the patients than that in the controls (P = 0.029). LVGU was inversely correlated with mutation heteroplasmy, glycated haemoglobin and fasting lactate in patients. The seven patients with mutation heteroplasmy ≥ 49% had 44% lower LVGU than the seven patients with heteroplasmy < 49%. This difference remained significant after adjustment for concurrent free fatty acid concentration or glycated haemoglobin or glucose uptake in skeletal muscle or all (p < 0.048 [All]). Patients with m.3243A > G had a lower stroke volume and a higher heart rate than the controls, whereas cardiac output and work were similar. Myocardial glucose uptake is not increased but decreased with a threshold effect pattern in patients with the m.3243A > G mutation. The glucose hypometabolism adds to the impaired cardiac energetics and likely contributes to the progression of the mitochondrial cardiomyopathy.
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http://dx.doi.org/10.1007/s10545-015-9865-1DOI Listing
January 2016

m.3243A>G mutation in mitochondrial DNA leads to decreased insulin sensitivity in skeletal muscle and to progressive beta-cell dysfunction.

Diabetes 2009 Mar 10;58(3):543-9. Epub 2008 Dec 10.

Turku PET Centre, University of Turku and Turku University Hospital, Turku, Finland.

Objective: To study insulin sensitivity and perfusion in skeletal muscle together with the beta-cell function in subjects with the m.3243A>G mutation in mitochondrial DNA, the most common cause of mitochondrial diabetes.

Research Design And Methods: We measured skeletal muscle glucose uptake and perfusion using positron emission tomography and 2-[18F]fluoro-2-deoxyglucose and [15O]H2O during euglycemic hyperinsulinemia in 15 patients with m.3243A>G. These patients included five subjects with no diabetes as defined by the oral glucose tolerance test (OGTT) (group 1), three with GHb <6.1% and newly found diabetes by OGTT (group 2), and seven with a previously diagnosed diabetes (group 3). Control subjects consisted of 13 healthy individuals who were similar to the carriers of m.3243A>G with respect to age and physical activity. Beta-cell function was assessed using the OGTT and subsequent mathematical modeling.

Results: Skeletal muscle glucose uptake was significantly lower in groups 1, 2, and 3 than in the control subjects. The glucose sensitivity of beta-cells in group 1 patients was similar to that of the control subjects, whereas in group 2 and 3 patients, the glucose sensitivity was significantly lower. The insulin secretion parameters correlated strongly with the proportion of m.3243A>G mutation in muscle.

Conclusions: Our findings show that subjects with m.3243A>G are insulin resistant in skeletal muscle even when beta-cell function is not markedly impaired or glucose control compromised. We suggest that both the skeletal muscle insulin sensitivity and the beta-cell function are affected before the onset of the mitochondrial diabetes caused by the m.3243A>G mutation.
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http://dx.doi.org/10.2337/db08-0981DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2646052PMC
March 2009

Functional evaluation of microvascular free flaps with positron emission tomography.

J Plast Reconstr Aesthet Surg 2006 ;59(2):158-65

Department of Otorhinolaryngology, Head and Neck Surgery, Turku University Central Hospital, FIN-20521 Turku, Finland.

Background: The aim of this study was to assess blood flow (BF) of microvascular free flaps studied with positron emission tomography (PET) in patients with head and neck squamous cell cancer (HNSCC) undergoing major radical surgery 3-4 weeks after high-dose radiotherapy.

Methods: Five patients underwent resection of the HNSCC of the oral cavity followed by microvascular reconstruction with a radial forearm flap. Regional BF in oral and neck tissues was measured with PET using radiolabelled water ([15O]H2O) twice (1-2 and 12-14 days, respectively) following radical surgery.

Results: In the first postoperative PET study, the median BF in the cutaneous flap area was 5.1 mL/100 g/min, and in the muscle contra-lateral to the recipient site 19.9 mL/100 g/min. A low flap-to-muscle BF ratio appeared to correlate with circulatory incongruity, and thus with poorer flap success. The follow-up study on the second postoperative week supported the results of the primary PET scan.

Conclusions: This pilot study suggests that PET using [15O]H2O is a feasible method to quantitatively evaluate BF of the whole free flap in patients operated on for oral
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http://dx.doi.org/10.1016/j.bjps.2005.04.016DOI Listing
June 2006