scholarly journals Association between breastfeeding and insulin sensitivity among young people with Type 1 and Type 2 diabetes: the SEARCH Nutrition Ancillary Study

2016 ◽  
Vol 33 (10) ◽  
pp. 1452-1455
Author(s):  
N. S. The ◽  
C. M. Shay ◽  
A. P. Lamichhane ◽  
T. L. Crume ◽  
J. L. Crandell ◽  
...  
Diabetes Care ◽  
2004 ◽  
Vol 27 (5) ◽  
pp. 1148-1152 ◽  
Author(s):  
W. A. Hunter ◽  
T. Cundy ◽  
D. Rabone ◽  
P. L. Hofman ◽  
M. Harris ◽  
...  

1993 ◽  
Vol 85 (1) ◽  
pp. 77-81 ◽  
Author(s):  
C. A. Abbott ◽  
M. I. MacKness ◽  
S. Kumar ◽  
A. O. Olukoga ◽  
C. Gordon ◽  
...  

1. The activity of serum butyrylcholinesterase (‘pseudocholinesterase’, EC3.1.1.8) was investigated in 56 patients with type 1 diabetes mellitus, 51 patients with type 2 diabetes mellitus and 101 healthy control subjects. 2. Butyrylcholinesterase activity was significantly elevated in both type 1 (8.10 ± 3.35 units/ml) and type 2 (7.22 ± 1.95 units/ml) diabetes compared with the control subjects (4.23 ± 1.89 units/ml) (P <0.001). 3. In the patients with type 1 and type 2 diabetes, serum butyrylcholinesterase activity was correlated with log serum fasting triacylglycerol concentration (r = 0.41 and r = 0.43, respectively, P <0.001). In the type 2 population serum butyrylcholinesterase activity was also correlated with insulin sensitivity (r = −0.51, P <0.001). 4. Serum butyrylcholinesterase activity was unrelated to age, gender, serum γ-glutamyltranspeptidase activity, body mass index, or treatment for diabetes in both the diabetic populations. 5. In 37 non-diabetic patients with butyrylcholinesterase deficiency serum triacylglycerol levels were in the normal range. 6. These results are consistent with the view that butyrylcholinesterase may have a role in the altered lipoprotein metabolism in hypertriglyceridaemia associated with insulin insensitivity or insulin deficiency in diabetes mellitus.


2021 ◽  
Vol 12 ◽  
Author(s):  
Dominik Pesta ◽  
Tomas Jelenik ◽  
Oana-Patricia Zaharia ◽  
Pavel Bobrov ◽  
Sven Görgens ◽  
...  

The rs540467 SNP in the NDUFB6 gene, encoding a mitochondrial complex I subunit, has been shown to modulate adaptations to exercise training. Interaction effects with diabetes mellitus remain unclear. We assessed associations of habitual physical activity (PA) levels with metabolic variables and examined a possible modifying effect of the rs540467 SNP. Volunteers with type 2 (n=242), type 1 diabetes (n=250) or normal glucose tolerance (control; n=139) were studied at diagnosis and subgroups with type 1 (n=96) and type 2 diabetes (n=95) after 5 years. Insulin sensitivity was measured by hyperinsulinemic-euglycemic clamps, oxygen uptake at the ventilator threshold (VO2AT) by spiroergometry and PA by questionnaires. Translational studies investigated insulin signaling and mitochondrial function in Ndufb6 siRNA-treated C2C12 myotubes, with electronic pulse stimulation (EPS) to simulate exercising. PA levels were 10 and 6%, VO2AT was 31% and 8% lower in type 2 and type 1 diabetes compared to control. Within 5 years, 36% of people with type 2 diabetes did not improve their insulin sensitivity despite increasing PA levels. The NDUFB6 rs540467 SNP modifies PA-mediated changes in insulin sensitivity, body composition and liver fat estimates in type 2 diabetes. Silencing Ndufb6 in myotubes reduced mitochondrial respiration and prevented rescue from palmitate-induced insulin resistance after EPS. A substantial proportion of humans with type 2 diabetes fails to respond to rising PA with increasing insulin sensitivity. This may at least partly relate to a polymorphism of the NDUFB6 gene, which may contribute to modulating mitochondrial function.Clinical Trial RegistrationClinicalTrials.gov, identifier NCT01055093. The trial was retrospectively registered on 25th of January 2010.


2016 ◽  
Vol 101 (5) ◽  
pp. 2130-2140 ◽  
Author(s):  
Birgit Knebel ◽  
Klaus Strassburger ◽  
Julia Szendroedi ◽  
Jorg Kotzka ◽  
Marsel Scheer ◽  
...  

Abstract Context: Insulin resistance reflects the inadequate insulin-mediated use of metabolites and predicts type 2 diabetes (T2D) but is also frequently seen in long-standing type 1 diabetes (T1D) and represents a major cardiovascular risk factor. Objective: We hypothesized that plasma metabolome profiles allow the identification of unique and common early biomarkers of insulin resistance in both diabetes types. Design, Setting, and Patients: Two hundred ninety-five plasma metabolites were analyzed by mass spectrometry from patients of the prospective observational German Diabetes Study with T2D (n = 244) or T1D (n = 127) and known diabetes duration of less than 1 year and glucose-tolerant persons (CON; n = 129). Abundance of metabolites was tested for association with insulin sensitivity as assessed by hyperinsulinemic-euglycemic clamps and related metabolic phenotypes. Main Outcomes Measures: Sixty-two metabolites with phenotype-specific patterns were identified using age, sex, and body mass index as covariates. Results: Compared with CON, the metabolome of T2D and T1D showed similar alterations in various phosphatidylcholine species and amino acids. Only T2D exhibited differences in free fatty acids compared with CON. Pairwise comparison of metabolites revealed alterations of 28 and 49 metabolites in T1D and T2D, respectively, when compared with CON. Eleven metabolites allowed differentiation between both diabetes types and alanine, α-amino-adipic acid, isoleucin, and stearic acid showed an inverse association with insulin sensitivity in both T2D and T1D combined. Conclusion: Metabolome analyses from recent-onset T2D and T1D patients enables identification of defined diabetes type-specific differences and detection of biomarkers of insulin sensitivity. These analyses may help to identify novel clinical subphenotypes diabetes.


2021 ◽  
Vol 9 (2) ◽  
pp. e002485
Author(s):  
Sasini Wijayaratna ◽  
Arier Lee ◽  
Hyun Young Park ◽  
Emmanuel Jo ◽  
Fiona Wu ◽  
...  

IntroductionYoung people with type 2 diabetes (T2D) develop complications earlier than those with type 1 diabetes (T1D) of comparable duration, but it is unclear why. This apparent difference in phenotype could relate to relative inequality.Research design and methodsCross-sectional study of young people referred to secondary diabetes services in Auckland, Aotearoa-New Zealand (NZ): 731 with T1D and 1350 with T2D currently aged <40 years, and diagnosed between 15 and 30 years. Outcome measures were risk factors for complications (glycemic control, urine albumin/creatinine ratio (ACR), cardiovascular disease (CVD) risk) in relation to a validated national index of deprivation (New Zealand Deprivation Index (NZDep)).ResultsYoung people with T2D were an average 3 years older than those with T1D but had a similar duration of diabetes. 71% of those with T2D were of Māori or Pasifika descent, compared with 24% with T1D (p<0.001). T1D cases were distributed evenly across NZDep categories. 78% of T2D cases were living in the lowest four NZDep categories (p<0.001). In both diabetes types, body mass index (BMI) increased progressively across the NZDep spectrum (p<0.002), as did mean glycated hemoglobin (HbA1c) (p<0.001), the prevalence of macroalbuminuria (p≤0.01), and CVD risk (p<0.001). Adjusting for BMI, diabetes type, and duration and age, multiple logistic regression revealed deprivation was the strongest risk factor for poorly controlled diabetes (defined as HbA1c >64 mmol/mol, >8%); OR 1.17, 95% CI 1.13 to 1.22, p<0.0001. Ordinal logistic regression showed each decile increase in NZDep increased the odds of a higher ACR by 11% (OR 1.11, 95% CI 1.06 to 1.16, p<0.001) following adjustment for BMI, blood pressure, diabetes type and duration, HbA1c, and smoking status. Multiple linear regression indicated a 4% increase in CVD risk for every decile increase in NZDep, regardless of diabetes type.ConclusionsThe apparent more aggressive phenotype of young-onset T2D is at least in part explicable by relative deprivation.


Sign in / Sign up

Export Citation Format

Share Document