ORCID Profile
0000-0002-8522-1288
Current Organisations
University of Helsinki
,
Helsinki University Central Hospital
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Publisher: Elsevier BV
Date: 04-2013
Abstract: The impact of diet on the gut microbiota has usually been assessed by subjecting people to the same controlled diet and thereafter following the shifts in the microbiota. In the present study, we used habitual dietary intake, clinical data, quantitative polymerase chain reaction, and denaturing gradient gel electrophoresis (DGGE) to characterize the stool microbiota of Finnish monozygotic twins. The effect of diet on the numbers of bacteria was described through a hierarchical linear mixed model that included the twin in iduals, stratified by body mass index, and their families as random effects. The abundance and ersity of the bacterial groups studied did not differ between normal-weight, overweight, and obese in iduals with the techniques used. Intakes of energy, monounsaturated fatty acids, n3 polyunsaturated fatty acids (PUFAs), n6 PUFAs, and soluble fiber had significant associations with the stool bacterial numbers (e.g., increased energy intake was associated with reduced numbers of Bacteroides spp.). In addition, co-twins with identical energy intake had more similar numbers and DGGE-profile ersities of Bacteroides spp. than did the co-twins with different intake. Moreover, the co-twins who ingested the same amounts of saturated fatty acids had very similar DGGE profiles of Bacteroides spp., whereas the co-twins with similar consumption of fiber had a very low bifidobacterial DGGE-profile similarity. In conclusion, our findings confirm that the diet plays an important role in the modulation of the stool microbiota, in particular Bacteroides spp. and bifidobacteria.
Publisher: Springer Science and Business Media LLC
Date: 20-10-2018
Publisher: Springer Science and Business Media LLC
Date: 19-04-2018
DOI: 10.1038/S41598-018-24634-2
Abstract: It is well established that boys are born heavier and longer than girls, but it remains unclear whether birth size in twins is affected by the sex of their co-twin. We conducted an in idual-based pooled analysis of 21 twin cohorts in 15 countries derived from the COllaborative project of Development of Anthropometrical measures in Twins (CODATwins), including 67,850 dizygotic twin in iduals. Linear regression analyses showed that boys having a co-twin sister were, on average, 31 g (95% CI 18 to 45) heavier and 0.16 cm (95% CI 0.045 to 0.274) longer than those with a co-twin brother. In girls, birth size was not associated (5 g birth weight 95% CI −8 to −18 and −0.089 cm birth length 95% CI −0.202 to 0.025) with the sex of the co-twin. Gestational age was slightly shorter in boy-boy pairs than in boy-girl and girl-girl pairs. When birth size was standardized by gestational age, the magnitude of the associations was attenuated in boys, particularly for birth weight. In conclusion, boys with a co-twin sister are heavier and longer at birth than those with a co-twin brother. However, these differences are modest and partly explained by a longer gestation in the presence of a co-twin sister.
Publisher: Cambridge University Press (CUP)
Date: 12-2015
DOI: 10.1017/THG.2015.83
Abstract: Twin pairs discordant for disease may help elucidate the epigenetic mechanisms and causal environmental factors in disease development and progression. To obtain the numbers of pairs, especially monozygotic (MZ) twin pairs, necessary for in-depth studies while also allowing for replication, twin studies worldwide need to pool their resources. The Discordant Twin (DISCOTWIN) consortium was established for this goal. Here, we describe the DISCOTWIN Consortium and present an analysis of type 2 diabetes (T2D) data in nearly 35,000 twin pairs. Seven twin cohorts from Europe (Denmark, Finland, Norway, the Netherlands, Spain, Sweden, and the United Kingdom) and one from Australia investigated the rate of discordance for T2D in same-sex twin pairs aged 45 years and older. Data were available for 34,166 same-sex twin pairs, of which 13,970 were MZ, with T2D diagnosis based on self-reported diagnosis and medication use, fasting glucose and insulin measures, or medical records. The prevalence of T2D ranged from 2.6% to 12.3% across the cohorts depending on age, body mass index (BMI), and national diabetes prevalence. T2D discordance rate was lower for MZ (5.1%, range 2.9–11.2%) than for same-sex dizygotic (DZ) (8.0%, range 4.9–13.5%) pairs. Across DISCOTWIN, 720 discordant MZ pairs were identified. Except for the oldest of the Danish cohorts (mean age 79), heritability estimates based on contingency tables were moderate to high (0.47–0.77). From a meta-analysis of all data, the heritability was estimated at 72% (95% confidence interval 61–78%). This study demonstrated high T2D prevalence and high heritability for T2D liability across twin cohorts. Therefore, the number of discordant MZ pairs for T2D is limited. By combining national resources, the DISCOTWIN Consortium maximizes the number of discordant MZ pairs needed for in-depth genotyping, multi-omics, and phenotyping studies, which may provide unique insights into the pathways linking genes to the development of many diseases.
Publisher: Public Library of Science (PLoS)
Date: 29-03-2012
Publisher: Springer Science and Business Media LLC
Date: 24-04-2014
Publisher: Oxford University Press (OUP)
Date: 23-04-2014
DOI: 10.1093/HMG/DDU183
Publisher: Public Library of Science (PLoS)
Date: 10-03-2011
Publisher: Informa UK Limited
Date: 09-2018
DOI: 10.2147/PRBM.S160355
Publisher: Springer Science and Business Media LLC
Date: 06-12-2021
DOI: 10.1038/S42255-021-00497-2
Abstract: White to brown/beige adipocytes conversion is a possible therapeutic strategy to tackle the current obesity epidemics. While mitochondria are key for energy dissipation in brown fat, it is unknown if they can drive adipocyte browning. Here, we show that the mitochondrial cristae biogenesis protein optic atrophy 1 (Opa1) facilitates cell-autonomous adipocyte browning. In two cohorts of patients with obesity, including weight discordant monozygotic twin pairs, adipose tissue OPA1 levels are reduced. In the mouse, Opa1 overexpression favours white adipose tissue expandability as well as browning, ultimately improving glucose tolerance and insulin sensitivity. Transcriptomics and metabolomics analyses identify the Jumanji family chromatin remodelling protein Kdm3a and urea cycle metabolites, including fumarate, as effectors of Opa1-dependent browning. Mechanistically, the higher cyclic adenosine monophosphate (cAMP) levels in Opa1 pre-adipocytes activate cAMP-responsive element binding protein (CREB), which transcribes urea cycle enzymes. Flux analyses in pre-adipocytes indicate that Opa1-dependent fumarate accumulation depends on the urea cycle. Conversely, adipocyte-specific Opa1 deletion curtails urea cycle and beige differentiation of pre-adipocytes, and is rescued by fumarate supplementation. Thus, the urea cycle links the mitochondrial dynamics protein Opa1 to white adipocyte browning.
Publisher: European Respiratory Society (ERS)
Date: 05-12-2013
DOI: 10.1183/09031936.00046213
Abstract: Several clinical studies suggest the involvement of premature ageing processes in chronic obstructive pulmonary disease (COPD). Using an epidemiological approach, we studied whether accelerated ageing indicated by telomere length, a marker of biological age, is associated with COPD and asthma, and whether intrinsic age-related processes contribute to the interin idual variability of lung function. Our meta-analysis of 14 studies included 934 COPD cases with 15 846 controls defined according to the Global Lungs Initiative (GLI) criteria (or 1189 COPD cases according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria), 2834 asthma cases with 28 195 controls, and spirometric parameters (forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC) of 12 595 in iduals. Associations with telomere length were tested by linear regression, adjusting for age, sex and smoking status. We observed negative associations between telomere length and asthma (β= -0.0452, p=0.024) as well as COPD (β= -0.0982, p=0.001), with associations being stronger and more significant when using GLI criteria than those of GOLD. In both diseases, effects were stronger in females than males. The investigation of spirometric indices showed positive associations between telomere length and FEV1 (p=1.07×10(-7)), FVC (p=2.07×10(-5)), and FEV1/FVC (p=5.27×10(-3)). The effect was somewhat weaker in apparently healthy subjects than in COPD or asthma patients. Our results provide indirect evidence for the hypothesis that cellular senescence may contribute to the pathogenesis of COPD and asthma, and that lung function may reflect biological ageing primarily due to intrinsic processes, which are likely to be aggravated in lung diseases.
Publisher: Oxford University Press (OUP)
Date: 19-05-2018
DOI: 10.1093/IJE/DYY081
Publisher: Springer Science and Business Media LLC
Date: 29-01-2012
DOI: 10.1038/NG.1073
Publisher: Public Library of Science (PLoS)
Date: 02-02-2016
Publisher: Springer Science and Business Media LLC
Date: 15-06-2014
DOI: 10.1038/NG.3011
Publisher: Oxford University Press (OUP)
Date: 19-03-2017
DOI: 10.1093/IJE/DYX031
Publisher: Wiley
Date: 20-05-2014
DOI: 10.1096/FJ.14-250167
Publisher: Cold Spring Harbor Laboratory
Date: 21-06-2018
DOI: 10.1101/353581
Abstract: Tobacco smoking is a risk factor for multiple diseases, including cardiovascular disease and diabetes. Many smoking-associated signals have been detected in the blood methylome, but the extent to which these changes are widespread to metabolically relevant tissues, and impact gene expression or cardio-metabolic health, remains unclear. We investigated smoking-associated DNA methylation and gene expression variation in adipose tissue from 542 healthy female twins with available well-characterized cardio-metabolic phenotype profiles. We identified 42 smoking-methylation and 42 smoking-expression signals, where five genes ( AHRR , CYP1A1 , CYP1B1 , CYTL1 , F2RL3 ) were both hypo-methylated and up-regulated in smokers. We replicated and validated a proportion of the signals in blood, adipose, skin, and lung tissue datasets, identifying tissue-shared effects. Smoking leaves systemic imprints on DNA methylation after smoking cessation, with stronger but shorter-lived effects on gene expression. We tested for associations between the observed smoking signals and several adiposity phenotypes that constitute cardio-metabolic disease risk. Visceral fat and android/gynoid ratio were associated with methylation at smoking-markers with functional impacts on expression, such as CYP1A1 , and in signals shared across tissues, such as NOTCH1 . At smoking-signals BHLHE40 and AHRR DNA methylation and gene expression levels in current smokers were predictive of future gain in visceral fat upon smoking cessation. Our results provide the first comprehensive characterization of coordinated DNA methylation and gene expression markers of smoking in adipose tissue, a subset of which link to human cardio-metabolic health and may give insights into the wide ranging risk effects of smoking across the body. Tobacco smoking is the strongest environmental risk factor for human disease. Here, we investigate how smoking systemically changes methylome and transcriptome signatures in multiple tissues in the human body. We observe strong and coordinated epigenetic and gene expression changes in adipose tissue, some of which are mirrored in blood, skin, and lung tissue. Smoking leaves a strong short-lived impact on gene expression levels, while methylation changes are long-lasting after smoking cessation. We investigated if these changes observed in a metabolically-relevant (adipose) tissue had impacts on human disease, and observed strong associations with cardio-metabolic disease traits. Some of the smoking signals could predict future gain in obesity and cardio-metabolic disease risk in current smokers who subsequently go on to quit smoking. Our results provide novel insights into understanding the widespread health consequence of smoking outside the lung.
Publisher: Springer Science and Business Media LLC
Date: 07-2015
DOI: 10.1038/NATURE14618
Publisher: Cambridge University Press (CUP)
Date: 10-2003
Publisher: Public Library of Science (PLoS)
Date: 31-10-2013
Publisher: Springer Science and Business Media LLC
Date: 07-07-2023
Publisher: Wiley
Date: 25-07-2014
DOI: 10.1111/OBR.12199
Publisher: Springer Science and Business Media LLC
Date: 30-03-2011
DOI: 10.1038/EJHG.2011.21
Publisher: Springer Science and Business Media LLC
Date: 31-12-2013
DOI: 10.1007/S00394-013-0645-0
Abstract: Study how the dietary intake affects the fecal microbiota of a group of obese in iduals after a 6-week very low-energy diet (VLED) and thereafter during a follow-up period of 5, 8, and 12 months. Additionally, we compared two different methods, fluorescent in situ hybridization (FISH) and real-time PCR (qPCR), for the quantification of fecal s les. Sixteen subjects participated in a 12-month dietary intervention which consisted of a VLED high in protein and low in carbohydrates followed by a personalized diet plan, combined with exercise and lifestyle counseling. Fecal s les were analyzed using qPCR, FISH, and denaturing gradient gel electrophoresis. The VLED affected the fecal microbiota, in particular bifidobacteria that decreased approximately two logs compared with the baseline numbers. The change in numbers of the bacterial groups studied followed the dietary intake and not the weight variations during the 12-month intervention. Methanogens were detected in 56% of the participants at every s ling point, regardless of the dietary intake. Moreover, although absolute numbers of comparable bacterial groups were similar between FISH and qPCR measurements, relative proportions were higher according to FISH results. Changes in the fecal microbial numbers of obese in iduals were primarily affected by the dietary intake rather than weight changes.
Publisher: American Diabetes Association
Date: 23-02-2015
DOI: 10.2337/DB14-0988
Abstract: Observational studies have reported different effects of adiposity on cardiovascular risk factors across age and sex. Since cardiovascular risk factors are enriched in obese in iduals, it has not been easy to dissect the effects of adiposity from those of other risk factors. We used a Mendelian randomization approach, applying a set of 32 genetic markers to estimate the causal effect of adiposity on blood pressure, glycemic indices, circulating lipid levels, and markers of inflammation and liver disease in up to 67,553 in iduals. All analyses were stratified by age (cutoff 55 years of age) and sex. The genetic score was associated with BMI in both nonstratified analysis (P = 2.8 × 10−107) and stratified analyses (all P & 3.3 × 10−30). We found evidence of a causal effect of adiposity on blood pressure, fasting levels of insulin, C-reactive protein, interleukin-6, HDL cholesterol, and triglycerides in a nonstratified analysis and in the & -year stratum. Further, we found evidence of a smaller causal effect on total cholesterol (P for difference = 0.015) in the ≥55-year stratum than in the & -year stratum, a finding that could be explained by biology, survival bias, or differential medication. In conclusion, this study extends previous knowledge of the effects of adiposity by providing sex- and age-specific causal estimates on cardiovascular risk factors.
Publisher: Elsevier BV
Date: 05-2018
Publisher: Wiley
Date: 07-08-2018
DOI: 10.1111/DOM.13466
Publisher: Springer Science and Business Media LLC
Date: 28-09-2020
Publisher: Elsevier BV
Date: 08-2017
Publisher: Springer Science and Business Media LLC
Date: 08-10-2020
Publisher: The Endocrine Society
Date: 2016
DOI: 10.1210/JC.2015-3095
Abstract: Sirtuins (SIRTs) regulate cellular metabolism and mitochondrial function according to the energy state of the cell reflected by NAD(+) levels. Our aim was to determine whether expressions of SIRTs and NAD(+) biosynthesis genes are affected by acquired obesity and how possible alterations are connected with metabolic dysfunction while controlling for genetic and familial factors. We studied a cross-sectional s le of 40 healthy pairs of monozygotic twins, including 26 pairs who were discordant for body mass index (within-pair difference > 3 kg/m(2)), from the FinnTwin12 and FinnTwin16 cohorts. Subcutaneous adipose tissue (SAT) transcriptomics was analyzed by using Affymetrix U133 Plus 2.0 chips, total SAT (poly-ADP) ribose polymerase (PARP) activity by an ELISA kit, body composition by dual-energy x-ray absorptiometry and magnetic resonance imaging/spectroscopy, and insulin sensitivity by an oral glucose tolerance test. SIRT1, SIRT3, SIRT5, NAMPT, NMNAT2, NMNAT3, and NRK1 expressions were significantly down-regulated and the activity of main cellular NAD(+) consumers, PARPs, trended to be higher in the SAT of heavier co-twins of body mass index-discordant pairs. Controlling for twin-shared factors, SIRT1, SIRT3, NAMPT, NMNAT3, and NRK1 were significantly negatively correlated with adiposity, SIRT1, SIRT5, NMNAT2, NMNAT3, and NRK1 were negatively correlated with inflammation, and SIRT1 and SIRT5 were positively correlated with insulin sensitivity. Expressions of genes involved in mitochondrial unfolded protein response were also significantly down-regulated in the heavier co-twins. Our data highlight a strong relationship of reduced NAD(+)/SIRT pathway expression with acquired obesity, inflammation, insulin resistance, and impaired mitochondrial protein homeostasis in SAT.
Publisher: Springer Science and Business Media LLC
Date: 27-04-2017
No related grants have been discovered for Kirsi Pietiläinen.