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Open access

Julia Otten, Mats Ryberg, Caroline Mellberg, Tomas Andersson, Elin Chorell, Bernt Lindahl, Christel Larsson, Jens Juul Holst and Tommy Olsson

Objective

To investigate how weight loss by different diets impacts postprandial levels of glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and glucagon.

Methods

In this single-centre, parallel group 2-year trial, 70 healthy postmenopausal obese women were randomised to the Paleolithic diet or a healthy control diet based on Nordic Nutrition Recommendations. Both diets were without calorie restriction. The primary outcome was the change in fat mass. Here, secondary analyses on GLP-1, GIP and glucagon measured during an OGTT are described.

Results

In the Paleolithic diet group, mean weight loss compared to baseline was 11% at 6 months and 10% at 24 months. In the control diet group, mean weight loss was 6% after 6 and 24 months (P = 0.0001 and P = 0.049 for the comparison between groups at 6 and 24 months respectively). Compared to baseline, the mean incremental area under the curve (iAUC) for GLP-1 increased by 34 and 45% after 6 and 24 months in the Paleolithic diet group and increased by 59% after 24 months in the control diet group. The mean iAUC for GIP increased only in the Paleolithic diet group. The area under the curve (AUC) for glucagon increased during the first 6 months in both groups. The fasting glucagon increase correlated with the β-hydroxybutyrate increase.

Conclusions

Weight loss caused an increase in postprandial GLP-1 levels and a further rise occurred during weight maintenance. Postprandial GIP levels increased only after the Paleolithic diet. Reduced postprandial glucagon suppression may be caused by a catabolic state.

Open access

Irina Bancos, Jon Hazeldine, Vasileios Chortis, Peter Hampson, Angela E Taylor, Janet M Lord and Wiebke Arlt

Restricted access

Maria Othelie Underdal, Øyvind Salvesen, Anne Schmedes, Marianne Skovsager Andersen and Eszter Vanky

Objective

To explore whether gestational prolactin and breast increase are markers of metabolic health in pregnancy and on long-term, in PCOS.

Design

Follow-up study. Women with PCOS, according to the Rotterdam criteria (n = 239), former participants of the randomized controlled trial (RCT) PregMet were invited, 131 participated in the current follow-up study, at mean 8 years after pregnancy.

Methods

Metformin 2000 mg/day or placebo from first trimester to delivery in the original RCT. No intervention in the current study.

Prolactin was analyzed in the first trimester and at gestational week 32 and metabolic characteristics which are part of the metabolic syndrome and measures of glucose homeostasis were examined. Metabolic health was also evaluated according to breast increase versus lack of breast increase during pregnancy.

Results

Prolactin increase in pregnancy was negatively correlated to BMI (P = 0.007) and systolic blood pressure (P ≤ 0.001) in gestational week 32. Prolactin at gestational week 32 was negatively correlated to BMI (P = 0.044) and visceral fat area (P = 0.028) at 8-year follow-up in an unadjusted model. Prolactin at gestational week 32 showed no associations to metabolic health at follow-up when baseline BMI was adjusted for. Women who reported lack of breast increase during pregnancy, had higher BMI (P = 0.034), waist-hip ratio (P = 0.004), visceral fat area (P = 0.050), total cholesterol (P = 0.022), systolic (P = 0.027) and diastolic blood pressure (P = 0.011) at 8-year follow-up.

Conclusion

High prolactin levels and breast increase in pregnancy were associated with a more favorable long-term metabolic health in women with PCOS. Both prolactin and breast increase may be mediated by gestational BMI.

Restricted access

Katrien Benhalima, Paul Van Crombrugge, Carolien Moyson, Johan Verhaeghe, Sofie Vandeginste, Hilde Verlaenen, Chris Vercammen, Toon Maes, Els Dufraimont, Christophe De Block, Yves Jacquemyn, Farah Mekahli, Katrien De Clippel, Annick Van Den Bruel, Anne Loccufier, Annouschka Laenen, Caro Minschart, Roland Devlieger and Chantal Mathieu

Objective

Since many European countries use risk factor screening for gestational diabetes mellitus (GDM), we aimed to determine the performance of selective screening for GDM based on the 2013 WHO criteria.

Design and methods

Overall, 1811 women received universal screening with a 75 g oral glucose tolerance test (OGTT) with GDM in 12.5% (n = 231) women based on the 2013 WHO criteria. We retrospectively applied different European selective screening guidelines to this cohort and evaluated the performance of different clinical risk factors to screen for GDM.

Results

By retrospectively applying the English, Irish, French and Dutch guidelines for selective screening, respectively 28.5% (n = 526), 49.7% (n = 916), 48.5% (n = 894) and 50.7% (n = 935) had at least one risk factor, with GDM prevalence of respectively 6.5% (n = 120), 7.9% (n = 146), 8.0% (n = 147) and 8.4% (n = 154). Using maternal age ≥30 and/or BMI ≥25 for screening, positive rate was 69.9% (n = 1288), GDM prevalence 10.2% (n = 188), sensitivity 81.4% (CI: 75.8–86.2%) and specificity 31.8% (CI: 29.5–34.1%). Adding other clinical risk factors did not improve detection. GDM women without risk factors had more neonatal hypoglycemia (14.4 vs 4.0%, P = 0.001) and labor inductions (39.7 vs 25.9%, P = 0.020) than normal-glucose tolerant women, and less cesarean sections than GDM women with risk factors (13.8 vs 31.0%, P = 0.010).

Conclusions

By applying selective screening by European guidelines, about 50% of women would need an OGTT with the lowest number of missed cases (33%) by the Dutch guidelines. Screening with age ≥30 years and/or BMI ≥25, reduced the number of missed cases to 18.6% but 70% would need an OGTT.

Restricted access

Elodie Fiot, Delphine Zénaty, Priscilla Boizeau, Jérémie Haignere, Sophie Dos Santos, Juliane Léger and the French Turner Syndrome Study Group

Objective

Turner Syndrome is associated with several phenotypic conditions associated with a higher risk of subsequent comorbidity. We aimed to evaluate the prevalence of congenital malformations and the occurrence of age-related comorbid conditions and to determine whether the frequencies of congenital and acquired conditions depend on X chromosome gene dosage, as a function of karyotype subgroup.

Design and methods

This national retrospective observational cohort study includes 1501 patients. We evaluated the prevalence of congenital malformations and the cumulative incidence of subsequent specific comorbidities at five-year intervals, from the ages of 10 to 30 years, with stratification by karyotype subgroup: 45,X (n = 549), 45,X/46,isoXq (n = 280), 46,X,r(X)/46,XX (n = 106), 45,X/46,XX (n = 221), presence of Y (n = 87).

Results

Median age was 9.4 (3.7–13.7) years at first evaluation and 16.8 (11.2–21.4) years at last evaluation. Congenital heart (18.9%) malformations were more frequent in 45,X patients, and congenital renal (17.2%) malformations were more frequent in 45,X, 45,X/46,isoXq and 46,X,r(X)/46,XX patients than in those with 45,X/46,XX mosaicism or a Y chromosome (P < 0.0001). The cumulative incidence of subsequent acquired conditions, such as thyroid disease, hearing loss, overweight/obesity, dyslipidemia and, to a lesser extent, celiac disease, glucose intolerance/type 2 diabetes, hypertension and liver dysfunction increased with age, but less markedly for patients with mosaicism than for those with other karyotypes. Patients with a ring chromosome were more prone to metabolic disorders.

Conclusion

These data suggest that X gene chromosome dosage, particularly for Xp genes, contributes to the risk of developing comorbidities.

Restricted access

Sergio Valdés, Viyey Doulatram-Gamgaram, Ana Lago, Francisca García Torres, Rocío Badía-Guillén, Gabriel Olveira, Albert Goday, Alfonso Calle-Pascual, Luis Castaño, Conxa Castell, Elías Delgado, Edelmiro Menendez, Josep Franch-Nadal, Sonia Gaztambide, Joan Girbés, Ramón Gomis, Emilio Ortega, José L Galán-García, Gabriel Aguilera-Venegas, Federico Soriguer and Gemma Rojo-Martínez

Objective

The activity of brown adipose tissue is sensitive to changes in ambient temperature. A lower exposure to cold could result in an increased risk of developing diabetes at population level, although this factor has not yet been sufficiently studied.

Design

We studied 5072 subjects, participants in a national, cross-sectional population-based study representative of the Spanish adult population (Di@bet.es study). All subjects underwent a clinical, demographic and lifestyle survey, a physical examination and blood sampling (75 g oral glucose tolerance test). Insulin resistance was estimated with the homeostasis model assessment (HOMA-IR). The mean annual temperature (°C) in each individual municipality was collected from the Spanish National Meteorology Agency.

Results

Linear regression analysis showed a significant positive association between mean annual temperature and fasting plasma glucose (β: 0.087, P < 0.001), 2 h plasma glucose (β: 0.049, P = 0.008) and HOMA-IR (β: 0.046, P = 0.008) in multivariate adjusted models. Logistic regression analyses controlled by multiple socio-demographic variables, lifestyle, adiposity (BMI) and geographical elevation showed increasing odds ratios for prediabetes (WHO 1999), ORs 1, 1.26 (0.95–1.66), 1.08 (0.81–1.44) and 1.37 (1.01–1.85) P for trend = 0.086, diabetes (WHO 1999) ORs 1, 1.05 (0.79–1.39), 1.20 (0.91–1.59) and 1.39 (1.02–1.90) P = 0.037, and insulin resistance (HOMA-IR ≥75th percentile of the non-diabetic population): ORs 1, 1.03 (0.82–1.30), 1.22 (0.96–1.55), 1.26 (0.98–1.63) (P for trend = 0.046) as the mean annual temperature (into quartiles) rose.

Conclusions

Our study reports an association between ambient temperature and the prevalence of dysglycemia and insulin resistance in Spanish adults, consistent with the hypothesis that a lower exposure to cold could be associated with a higher risk of metabolic derangements.

Restricted access

Susan Kralisch, Annett Hoffmann, Nora Klöting, Armin Frille, Hartmut Kuhn, Marcin Nowicki, Sabine Paeschke, Anette Bachmann, Matthias Blüher, Ming-Zhi Zhang, Raymond C. Harris, Michael Stumvoll, Mathias Fasshauer and Thomas Ebert

Objective: Neuregulin 4 (Nrg4) has recently been introduced as a novel brown adipose tissue (BAT)-secreted adipokine with beneficial metabolic effects in mice. However, regulation of Nrg4 in end-stage kidney disease (ESKD) and type 2 diabetes mellitus (T2DM) has not been elucidated, so far.

Design/Methods: Serum Nrg4 levels were quantified by ELISA in 60 subjects with ESKD on chronic hemodialysis as compared to 60 subjects with an estimated glomerular filtration rate >50 ml/min/1.73m² in a cross-sectional cohort. Within both groups, about half of the patients had a T2DM. Furthermore, mNrg4 mRNA expression was determined in two mouse models of diabetic kidney disease (DKD) as compared to two different groups of non-diabetic control mice. Moreover, mNrg4 mRNA expression was investigated in murine brown and white adipocytes, as well as hepatocytes, after treatment with the uremic toxin indoxyl sulfate.

Results: Median serum Nrg4 was significantly lower in patients with ESKD compared to controls and the adipokine was independently associated with a beneficial renal, glucose, and lipid profile. In mice with DKD, mNrg4 mRNA expression was decreased in all adipose tissue depots compared to control mice. The uremic toxin indoxyl sulfate did not significantly alter mNrg4 mRNA expression in adipocytes and hepatocytes, in vitro.

Conclusions: Circulating Nrg4 is independently associated with a preserved renal function and mNrg4 mRNA expression is reduced in adipose tissue depots of mice with DKD. The BAT-secreted adipokine is further associated with a beneficial glucose and lipid profile supporting Nrg4 as potential treatment target in metabolic and renal disease states.

Free access

Mario Rotondi, Andrea Carbone, Francesca Coperchini, Rodolfo Fonte and Luca Chiovato

IgG4-related disease (IgG4-RD) is fibro-inflammatory, immune-mediated, systemic disease recognized as a defined clinical condition only in 2001. The prevalence of IgG4-RD is 6/100 000, but it is likely to be underestimated due to insufficient awareness of the disease. The diagnostic approach is complex because of the heterogeneity of clinical presentation and because of rather variable diagnostic criteria. Indeed, high concentrations of IgG4 in tissue and serum are not a reliable diagnostic marker. The spectrum of IgG4-RD also includes well-known thyroid diseases including Riedel’s thyroiditis, Hashimoto’s thyroiditis and its fibrotic variant, Graves’ disease and Graves’ orbitopathy. Results from clinical studies indicate that a small subset of patients with the above-mentioned thyroid conditions present some features suggestive for IgG4-RD. However, according to more recent views, the use of the term thyroid disease with an elevation of IgG4 rather than IgG4-related thyroid diseases would appear more appropriate. Nevertheless, the occurrence of high IgG4 levels in patients with thyroid disease is relevant due to peculiarities of their clinical course.

Restricted access

Hanne L Gulseth, Ingrid M F Gjelstad, Audrey C Tiereny, Danielle McCarthy, Julie A Lovegrove, Catherine Defoort, Ellen E Blaak, Jose Lopez-Miranda, Aldona Dembinska-Kiec, Ulf Risérus, Helen M Roche, Christian A Drevon and Kåre I Birkeland

Objective

Impaired insulin secretion and action contribute to the development of type 2 diabetes. Dietary fat modification may improve insulin sensitivity, whereas the effect on insulin secretion is unclear. We investigated the effect of dietary fat modification on insulin secretion in subjects with the metabolic syndrome.

Design

In a 12-week pan-European parallel, randomized controlled dietary intervention trial (LIPGENE), 486 subjects were assigned to four isoenergetic diets: high-fat diets rich in saturated fat (HSFA) or monounsaturated fat (HMUFA) or low-fat, high-complex carbohydrate diets with (LFHCC n-3) or without (LFHCC control) 1.2 g/day of n-3 PUFA supplementation. Insulin secretion was estimated as acute insulin response to glucose (AIRg) and disposition index (DI), modeled from an intravenous glucose tolerance test.

Results

There were no overall effect of the dietary intervention on AIRg and DI in the total cohort, in neither the high-fat nor LFHCC groups. We observed significant diet*fasting glucose category interactions for AIRg (P = 0.021) and DI (P = 0.001) in the high-fat groups. In subjects with normal fasting glucose and preserved first phase insulin secretion, the HMUFA diet increased, whereas the HSFA diet reduced AIRg (P = 0.015) and DI (P = 0.010).

Conclusions

The effects of dietary fat modification on insulin secretion were minor, and only evident in normoglycemic subjects. In this case, the HMUFA diet improved AIRg and DI, as compared to the HSFA diet.

Restricted access

Andreas Stomby, Alireza Salami, Per Dahlqvist, Johan Arild Evang, Mats Ryberg, Jens Bollerslev, Tommy Olsson, Gudmundur Johannsson and Oskar Ragnarsson

Objective

Cushing’s syndrome is associated with long-term cognitive deficits and affective symptoms such as depression and anxiety. The alterations in brain function underlying these deficits after Cushing’s syndrome are unclear and therefore we aimed to explore alterations in resting-state functional connectivity in patients with Cushing’s syndrome in remission.

Design

Cross-sectional case–control study.

Methods

Nineteen women with Cushing’s syndrome in remission for a median time of 7 years (IQR: 6–10) and a mean age of 45 years were included at three university clinics. These patients and 38 age-matched female controls underwent brain imaging at a single center. The main outcome measure was functional connectivity at rest, measured with functional magnetic resonance imaging.

Results

The medial temporal lobe (MTL) and prefrontal cortex networks, exhibited elevated functional connectivity among patients compared to controls. The degree of elevated functional connectivity in the MTL was negatively associated with time in remission.

Conclusions

Resting-state functional connectivity within glucocorticoid receptor-rich regions, particularly the MTL and medial prefrontal cortex, was increased in patients. These differences in connectivity may provide a neural basis for the cognitive deficits and affective symptoms commonly experienced by patients with Cushing’s syndrome in remission.