Glucose and Insulin Metabolism in Twins: Influence of Zygosity and Birth Weight

Twin Research ◽  
2001 ◽  
Vol 4 (5) ◽  
pp. 350-355 ◽  
Author(s):  
Pernille Poulsen ◽  
Allan Vaag
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Intolerance ◽  
Twin Studies ◽  
Metabolic Effects ◽  
Diabetes Research ◽  
Relative Role ◽  
Intrauterine Environment ◽  
Dizygotic Twins

AbstractSeveral epidemiological and metabolic studies have demonstrated an impact of the intrauterine environment on the development of disease in adult life, including Type 2 diabetes and glucose intolerance. Our finding of lower birth weights among monozygotic diabetic twins compared to their non-diabetic genetically identical co-twins confirms this association and, furthermore, eliminates the possibility that the association could be explained solely by common genes leading to both impaired intrauterine growth and increased risk of Type 2 diabetes. Due to an often shared placenta monozygotic twins may experience a more adverse intrauterine environment compared to dizygotic twins and may therefore be more prone to develop various metabolic abnormalities. Our findings of a higher glucose and insulin profile after oral glucose ingestion, and recently lower insulin-stimulated glucose uptake — indicating glucose intolerance and insulin resistance — among monozygotic compared to dizygotic twins may to some extent question the validity of classical twin studies in diabetes research where equal environmental influences in monozygotic and dizygotic twins is assumed. The potential role of an adverse intrauterine environment in causing Type 2 diabetes in humans, may to some degree alter our conception of the twin model in diabetes research including the interpretation of aetiological conclusions reached in previous classical twin studies of diabetes. However, our present knowledge is far too insufficient to discard the results from classical twin studies concerning the relative role of genes versus environment for the development of diabetes and its metabolic effects.

scholarly journals The Role of Low-calorie Sweeteners in Diabetes

2013 ◽  
Vol 09 (01) ◽  
pp. 13 ◽  
Author(s):  
Craig A Johnston ◽  
Brian Stevens ◽  
John P Foreyt ◽  
◽  
◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Diabetes Prevention ◽  
Caloric Intake ◽  
Diabetes Research ◽  
Added Sugars ◽  
Low Calorie ◽  
Dietary Preferences ◽  
Health Goals

As the incidence and prevalence of type 2 diabetes continue to rise, the identification of components that contribute to or are associated with this disease has become a priority. One of the main factors that has been linked to type 2 diabetes is excessive weight gain, and reduction in weight has been recommended for both diabetes prevention and management. Low-calorie sweeteners (LCS) provide an alternative to added sugars and may facilitate weight loss or maintenance by limiting caloric intake. Considerable attention has been given to the role of LCS and their relationship to type 2 diabetes. Research suggests that LCS can serve an important role in diabetes prevention and management. Substituting sugars with LCS provides patients with type 2 diabetes considerable flexibility in their health goals and personal dietary preferences.

scholarly journals Epigenetics and gestational diabetes: a review of epigenetic epidemiology studies and their use to explore epigenetic mediation and improve prediction

Diabetologia ◽  
2019 ◽  
Vol 62 (12) ◽  
pp. 2171-2178 ◽  
Author(s):  
Hannah R. Elliott ◽  
Gemma C. Sharp ◽  
Caroline L. Relton ◽  
Deborah A. Lawlor
Keyword(s):  
Type 2 Diabetes ◽  
Dna Methylation ◽  
Gestational Diabetes ◽  
Histone Modification ◽  
Diabetes Research ◽  
Epigenetic Mechanisms ◽  
Epigenetic Epidemiology ◽  
Epigenetic Biomarkers

Abstract Epigenetics encapsulates a group of molecular mechanisms including DNA methylation, histone modification and microRNAs (miRNAs). Gestational diabetes (GDM) increases the risk of adverse perinatal outcomes and is associated with future offspring risk of obesity and type 2 diabetes. It has been hypothesised that epigenetic mechanisms mediate an effect of GDM on offspring adiposity and type 2 diabetes and this could provide a modifiable mechanism to reduce type 2 diabetes in the next generation. Evidence for this hypothesis is lacking. Epigenetic epidemiology could also contribute to reducing type 2 diabetes by identifying biomarkers that accurately predict risk of GDM and its associated future adverse outcomes. We reviewed published human studies that explored associations between any of maternal GDM, type 2 diabetes, gestational fasting or post-load glucose and any epigenetic marker (DNA methylation, histone modification or miRNA). Of the 81 relevant studies we identified, most focused on the potential role of epigenetic mechanisms in mediating intrauterine effects of GDM on offspring outcomes. Studies were small (median total number of participants 58; median number of GDM cases 27) and most did not attempt replication. The most common epigenetic measure analysed was DNA methylation. Most studies that aimed to explore epigenetic mediation examined associations of in utero exposure to GDM with offspring cord or infant blood/placenta DNA methylation. Exploration of any causal effect, or effect on downstream offspring outcomes, was lacking. There is a need for more robust methods to explore the role of epigenetic mechanisms as possible mediators of effects of exposure to GDM on future risk of obesity and type 2 diabetes. Research to identify epigenetic biomarkers to improve identification of women at risk of GDM and its associated adverse (maternal and offspring) outcomes is currently rare but could contribute to future tools for accurate risk stratification.

Relative role of major risk factors for Type 2 diabetes development in the historical cohort of the Brisighella Heart Study: an 8-year follow-up

2005 ◽  
Vol 22 (9) ◽  
pp. 1263-1266 ◽  
Author(s):  
A. F. G. Cicero ◽  
A. Dormi ◽  
S. Nascetti ◽  
M. P. Panourgia ◽  
E. Grandi ◽  
...  
Keyword(s):  
Risk Factors ◽  
Type 2 Diabetes ◽  
Relative Role ◽  
Historical Cohort ◽  
Heart Study ◽  
Diabetes Development

scholarly journals The Role of Low-calorie Sweeteners in Diabetes

2010 ◽  
Vol 9 (2) ◽  
pp. 96 ◽  
Author(s):  
Craig A Johnston ◽  
Brian Stevens ◽  
John P Foreyt ◽  
◽  
◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Diabetes Prevention ◽  
Caloric Intake ◽  
Diabetes Research ◽  
Added Sugars ◽  
Low Calorie ◽  
Dietary Preferences ◽  
Health Goals

As the incidence and prevalence of type 2 diabetes continue to rise, the identification of components that contribute to or are associated with this disease has become a priority. One of the main factors that has been linked to type 2 diabetes is excessive weight gain, and reduction in weight has been recommended for both diabetes prevention and management. Low-calorie sweeteners (LCS) provide an alternative to added sugars and may facilitate weight loss or maintenance by limiting caloric intake. Considerable attention has been given to the role of LCS and their relationship to type 2 diabetes. Research suggests that LCS can serve an important role in diabetes prevention and management. Substituting sugars with LCS provides patients with type 2 diabetes considerable flexibility in their health goals and personal dietary preferences.

scholarly journals The role of macrophage migration inhibitory factor in obesity-associated type 2 diabetes in mice

2013 ◽  
Vol 65 (2) ◽  
pp. 499-505 ◽  
Author(s):  
Tamara Saksida ◽  
Stanislava Stosic-Grujicic ◽  
Ivana Stojanovic
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Intolerance ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Clinical Signs ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Deficient Mice

Macrophage migration inhibitory factor (MIF) is implicated in the pathogenesis of several inflammationrelated diseases, including obesity and type 2 diabetes (T2D). However, MIF deficiency itself promotes obesity and glucose intolerance in mice. Here we show that the introduction of a high-fat diet (HFD) further aggravates the parameters of obesity-associated T2D: weight gain and glucose intolerance. Furthermore, in contrast to MIF-KO mice on standard chow, HFD-fed MIF-KO mice develop insulin resistance. Although the clinical signs of obesity-associated T2D are upgraded, inflammation in MIF-deficient mice on HFD is significantly lower. These results imply that MIF possesses a complex role in glucose metabolism and the development of obesity-related T2D. However, the downregulation of inflammation upon MIF inhibition could be a useful tool in short-term T2D therapy for preventing pancreatic islet deterioration.

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