| 861. |
- Romaguera, D., et al.
(författare)
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Consumption of sweet beverages and type 2 diabetes incidence in European adults: results from EPIC-InterAct
- 2013
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Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 1432-0428 .- 0012-186X. ; 56:7, s. 1520-1530
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Tidskriftsartikel (refereegranskat)abstract
- Consumption of sugar-sweetened beverages has been shown, largely in American populations, to increase type 2 diabetes incidence. We aimed to evaluate the association of consumption of sweet beverages (juices and nectars, sugar-sweetened soft drinks and artificially sweetened soft drinks) with type 2 diabetes incidence in European adults. We established a case-cohort study including 12,403 incident type 2 diabetes cases and a stratified subcohort of 16,154 participants selected from eight European cohorts participating in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. After exclusions, the final sample size included 11,684 incident cases and a subcohort of 15,374 participants. Cox proportional hazards regression models (modified for the case-cohort design) and random-effects meta-analyses were used to estimate the association between sweet beverage consumption (obtained from validated dietary questionnaires) and type 2 diabetes incidence. In adjusted models, one 336 g (12 oz) daily increment in sugar-sweetened and artificially sweetened soft drink consumption was associated with HRs for type 2 diabetes of 1.22 (95% CI 1.09, 1.38) and 1.52 (95% CI 1.26, 1.83), respectively. After further adjustment for energy intake and BMI, the association of sugar-sweetened soft drinks with type 2 diabetes persisted (HR 1.18, 95% CI 1.06, 1.32), but the association of artificially sweetened soft drinks became statistically not significant (HR 1.11, 95% CI 0.95, 1.31). Juice and nectar consumption was not associated with type 2 diabetes incidence. This study corroborates the association between increased incidence of type 2 diabetes and high consumption of sugar-sweetened soft drinks in European adults.
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| 862. |
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| 863. |
- Rorsman, Patrik, et al.
(författare)
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Insulin granule dynamics in pancreatic beta cells
- 2003
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Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 1432-0428 .- 0012-186X. ; 46:8, s. 1029-1045
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Forskningsöversikt (refereegranskat)abstract
- Glucose-induced insulin secretion in response to a step increase in blood glucose concentrations follows a biphasic time course consisting of a rapid and transient first phase followed by a slowly developing and sustained second phase. Because Type 2 diabetes involves defects of insulin secretion, manifested as a loss of first phase and a reduction of second phase, it is important to understand the cellular mechanisms underlying biphasic insulin secretion. Insulin release involves the packaging of insulin in small (diameter approximate to0.3 mum) secretory granules, the trafficking of these granules to the plasma membrane, the exocytotic fusion of the granules with the plasma membrane and eventually the retrieval of the secreted membranes by endocytosis. Until recently, studies on insulin secretion have been confined to the appearance of insulin in the extracellular space and the cellular events preceding exocytosis have been inaccessible to more detailed analysis. Evidence from a variety of secretory tissues, including pancreatic islet cells suggests, however, that the secretory granules can be functionally divided into distinct pools that are distinguished by their release competence and/or proximity to the plasma membrane. The introduction of fluorescent proteins that can be targeted to the secretory granules, in combination with the advent of new techniques that allow real-time imaging of granule trafficking in living cells (granule dynamics), has led to an explosion of our knowledge of the pre-exocytotic and post-exocytotic processes in the beta cell. Here we discuss these observations in relation to previous functional and ultra-structural data as well as the secretory defects of Type 2 diabetes.
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| 864. |
- Rosengren, Annika, 1951, et al.
(författare)
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Cardiovascular outcomes in type 1 and type 2 diabetes
- 2023
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Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 0012-186X .- 1432-0428. ; 66:3, s. 425-437
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Forskningsöversikt (refereegranskat)abstract
- Diabetes is one of the most prevalent cardiometabolic disorders on the planet. Type 1 diabetes accounts for only a minority of all cases (recently estimated to be similar to 2% globally); however, since this is a disorder with an early onset, many people live with type 1 diabetes for a long time. CVD and premature death are the main long-term outcomes for both types of diabetes; however, the type of diabetes that carries the highest risk of these outcomes is a controversial topic and has not been widely studied. Because of the association between diabetes and CVD, the rise in type 2 diabetes prevalence over the past decades has huge effects on global health. The excess risk in people with diabetes compared with those without depends, to a large extent, on the presence of other factors, such as general cardiovascular risk factors (e.g. elevated LDL-cholesterol, hypertension and smoking) and also factors that are more specific to diabetes (e.g. HbA1c, and micro- and macroalbuminuria). Some contributory factors are modifiable, while others are not, such as age, sex and type of diabetes. Older people with type 2 diabetes who have risk factors that are under control can achieve levels of CVD risk that are similar to that of the general population, while younger individuals with type 1 diabetes are mostly unable to achieve similar levels of risk, probably because of long and cumulative exposure to raised blood glucose levels. Despite reports of declining rates of CVD among people with type 1 and type 2 diabetes, rising rates of both types of diabetes lead to a continuing rise in the number of people with cardiometabolic disorders worldwide, offsetting the progress made in many countries. Comparison between individuals with type 1 and type 2 diabetes with respect to risk of CVD is fraught with difficulties and highly dependent on other, concomitant factors, some of which are modifiable and others not. Nonetheless, as a whole, what matters most in determining the management of diabetes is absolute risk and lifetime risk. Life-long efforts to achieve glycaemic control, control of lipids and hypertension, and not smoking are key to prevention, with a healthy lifestyle and pharmacological therapy to be implemented as needed.
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| 865. |
- Rosengren, Annika, 1951, et al.
(författare)
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Excess risk of hospitalisation for heart failure among people with type 2 diabetes
- 2018
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Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 1432-0428 .- 0012-186X. ; 61:11, s. 2300-09
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Tidskriftsartikel (refereegranskat)abstract
- AIMS/HYPOTHESIS: Type 2 diabetes is an established risk factor for heart failure, but age-specific data are sparse. We aimed to determine excess risk of heart failure, based on age, glycaemic control and kidney function in comparison with age- and sex-matched control individuals from the general population. METHODS: Individuals with type 2 diabetes registered in the Swedish National Diabetes Registry 1998-2012 (n = 266,305) were compared with age-, sex- and county-matched control individuals without diabetes (n = 1,323,504), and followed over a median of 5.6 years until 31 December 2013. RESULTS: We identified 266,305 individuals with type 2 diabetes (mean age 62.0 years, 45.3% women) and 1,323,504 control individuals. Of the individuals with type 2 diabetes and control individuals, 18,715 (7.0%) and 50,157 (3.8%) were hospitalised with a diagnosis of heart failure, respectively. Comparing individuals with diabetes with those in the control group, men and women with type 2 diabetes who were younger than 55 years of age had HRs for hospitalisation for heart failure of 2.07 (95% CI 1.73, 2.48) and 4.59 (95% CI 3.50, 6.02), respectively, using analyses adjusted for socioeconomic variables and associated conditions. Younger age, poorer glycaemic control and deteriorating renal function were all associated with increased excess risk of heart failure in those with type 2 diabetes compared with the control group. However, people with diabetes who were >/=75 years and without albuminuria or with good glycaemic control (HbA1c
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| 866. |
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| 867. |
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| 868. |
- Rothacker, K. M., et al.
(författare)
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Acute hyperglycaemia does not have a consistent adverse effect on exercise performance in recreationally active young people with type 1 diabetes: a randomised crossover in-clinic study
- 2021
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Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 0012-186X .- 1432-0428. ; 64:8, s. 1737-174
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Tidskriftsartikel (refereegranskat)abstract
- Aims/hypothesis In individuals with type 1 diabetes, chronic hyperglycaemia impairs aerobic fitness. However, the effect of acute marked hyperglycaemia on aerobic fitness is unclear, and the impact of insulin level has not been examined. In this study, we explored if acute hyperglycaemia with higher or low insulin levels affects (V) over dotO(2peak) and other exercise performance indicators in individuals with type 1 diabetes. Methods Eligible participants were aged 14 to 30 years, with complication-free, type 1 diabetes and HbA(1c) <= 75 mmol/mol (<= 9%). Participants exercised in a clinical laboratory under three clamp (constant insulin, variable glucose infusion) conditions: euglycaemia (5mmol/l) with 20mU [m(2) BSA](-1) min(-1) insulin (where BSA is body surface area) (Eu20); hyperglycaemia (17mmol/l) with 20 mU [m(2) BSA](-1) min(-1) insulin (Hyper20); and hyperglycaemia (17 mmol/l) with mU [5 m(2) BSA](-1) min(-1) insulin (Hyper5) on separate days. Participants and the single testing assessor were blinded to condition, with participants allocated to randomised testing condition sequences as they were consecutively recruited. Standardised testing (in order) conducted on each of the three study days included: triplicate 6 second sprint cycling, grip strength, single leg static balance, vertical jump and modified Star Excursion Balance Test, ten simple and choice reaction times and one cycle ergometer (V) over dotO(2peak) test. The difference between conditions in the aforementioned testing measures was analysed, with the primary outcome being the difference in (V) over dotO(2peak). Results Twelve recreationally active individuals with type 1 diabetes (8 male, mean +/- SD 17.9 +/- 3.9 years, HbA(1c) 61 +/- 11 mmol/mol [7.7 +/- 1.0%], 7 +/- 3 h exercise/week) were analysed. Compared with Eu20, (V) over dotO(2peak) was lower in Hyper20 (difference 0.17 l/min [95% CI 0.31, 0.04; p = 0.02] 6.6% of mean Eu20 level), but Hyper5 was not different (p = 0.39). Comparedwith Eu20, sprint cycling peak power was not different in Hyper20 (p = 0.20), but was higher in Hyper5 (64 W [95% CI 13, 115; p = 0.02] 13.1%). Hyper20 reaction times were not different (simple: p = 0.12) but Hyper5 reaction times were slower (simple: 11 milliseconds [95% CI 1, 22; p = 0.04] 4.7%) than Eu20. No differences between Eu20 and either hyperglycaemic condition were observed for the other testing measures (p > 0.05). Conclusions/interpretation Acute marked hyperglycaemia in the higher but not low insulin state impaired (V) over dotO(2peak) but to a small extent. Acute hyperglycaemia had an insulin-dependent effect on sprint cycling absolute power output and reaction time but with differing directionality (positive for sprint cycling and negative for reaction time) and no effect on the other indicators of exercise performance examined. We find that acute hyperglycaemia is not consistently adverse and does not impair overall exercise performance to an extent clinically relevant for recreationally active individuals with type 1 diabetes. .
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| 869. |
- Rotter Sopasakis, Victoria, 1972, et al.
(författare)
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Short-term infusion of interleukin-6 does not induce insulin resistance in vivo or impair insulin signalling in rats
- 2004
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Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 0012-186X .- 1432-0428. ; 47:11, s. 1879-87
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Tidskriftsartikel (refereegranskat)abstract
- AIMS/HYPOTHESIS: Interleukin-6 has been implicated in the insulin resistance associated with obesity and impaired glucose tolerance. Previous studies in vitro have shown that IL-6 rapidly (1-2 h) impairs cellular insulin signalling and action through an increased expression of suppressor of cytokine signalling (SOCS)-3. In the present study, IL-6 or saline was infused in rats that were simultaneously in a state of hyperinsulinaemia. Muscle, liver and adipose tissue were excised after 2 h to examine potential effects on insulin signalling or gene expression. METHODS: The rats were infused with IL-6 or saline during a euglycaemic-hyperinsulinaemic clamp and the glucose infusion rate was measured after 90 to 120 min. Signal transducer and activator of transcription (STAT)3 phosphorylation and insulin-stimulated tyrosine phosphorylation of the insulin receptors and IRS were measured with immunoblotting and gene expression through real-time PCR. RESULTS: No inhibitory effect of IL-6 on insulin-stimulated whole-body glucose uptake was seen in spite of high circulating levels of IL-6 (0.85+/-0.08 nmol/l). Tyrosine phosphorylation of the insulin receptors and IRS was also unchanged in the liver, skeletal muscles and adipose tissue. However, tyrosine phosphorylation of STAT3 was increased in all tissues, showing that IL-6 signalling was activated. IL-6 mRNA tended to increase, while GLUT4, peroxisome proliferator-activated receptor-gamma coactivator-1 (PGC-1) and adiponectin gene expression were unchanged. CONCLUSIONS/INTERPRETATION: Infusion of IL-6 for 120 min in rats during euglycaemic-hyperinsulinaemic conditions did not alter the effect of insulin on whole-body glucose homeostasis, plasma adiponectin levels or insulin signalling in target tissues. Thus, the acute effects of IL-6, associated with SOCS-3 induction, do not lead to whole-body insulin resistance. These data further underscore the importance of the chronic, and potentially tissue-specific effects of IL-6 on insulin signalling and action.
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| 870. |
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