Seasonal Variation of HbA1c in Intensive Treatment of Children with Type 1 Diabetes

Nordfeldt, S.; Ludvigsson, Johnny

doi:10.1515/jpem.2000.13.5.529

Cited by 33 publications

(27 citation statements)

References 16 publications

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“…Furthermore, over a 2-year period it has been demonstrated for both hemispheres that in cooler months HbA1c is higher than in warmer months (Higgins et al, 2009). Swedish adults as well as American and Swedish children with T1DM revealed a similar distribution of HbA1c (Asplund, 1997;Hill, Peters, Thompson, Matthews, & Hindmarsh, 2013;Norfeldt & Ludvigsson, 2000) with lower HbA1c in summer than in winter. Children with larger seasonal variations showed an increased risk for SH (Norfeldt & Ludvigsson, 2000).…”

Section: Discussionmentioning

confidence: 79%

Accumulation of severe hypoglycemia at weekends and in warm seasons in patients with type 1 diabetes but not with type 2 diabetes

Holstein

Wohland

Patzer

et al. 2016

Journal of Diabetes and its Complications

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Section: Discussionmentioning

confidence: 79%

Accumulation of severe hypoglycemia at weekends and in warm seasons in patients with type 1 diabetes but not with type 2 diabetes

Holstein

Wohland

Patzer

et al. 2016

Journal of Diabetes and its Complications

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“…potentiating insulin resistance). Moreover, it must be appreciated that this seasonal mechanism for regulating metabolism that has been preserved over hundreds of millions of years of evolution is also manifested in man, as multiple studies have clearly demonstrated [66][67][68][69][70][71][72][73][74][75].…”

Section: Role Of the Biological Clock (Scn) And Circadian Rhythms In mentioning

confidence: 99%

Bromocriptine-QR therapy for the management of type 2 diabetes mellitus: developmental basis and therapeutic profile summary

Raskin

Cincotta

2016

Expert Review of Endocrinology & Metabolism

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An extended series of studies indicate that endogenous phase shifts in circadian neuronal input signaling to the biological clock system centered within the hypothalamic suprachiasmatic nucleus (SCN) facilitates shifts in metabolic status. In particular, a diminution of the circadian peak in dopaminergic input to the peri-SCN facilitates the onset of fattening, insulin resistance and glucose intolerance while reversal of low circadian peak dopaminergic activity to the peri-SCN via direct timed dopamine administration to this area normalizes the obese, insulin resistant, glucose intolerant state in high fat fed animals. Systemic circadian-timed daily administration of a potent dopamine D2 receptor agonist, bromocriptine, to increase diminished circadian peak dopaminergic hypothalamic activity across a wide variety of animal models of metabolic syndrome and type 2 diabetes mellitus (T2DM) results in improvements in the obese, insulin resistant, glucose intolerant condition by improving hypothalamic fuel sensing and reducing insulin resistance, elevated sympathetic tone, and leptin resistance. A circadian-timed (within 2 hours of waking in the morning) once daily administration of a quick release formulation of bromocriptine (bromocriptine-QR) has been approved for the treatment of T2DM by the U.S. Food and Drug Administration. Clinical studies with such bromocriptine-QR therapy (1.6 to 4.8 mg/day) indicate that it improves glycemic control by reducing postprandial glucose levels without raising plasma insulin. Across studies of various T2DM populations, bromocriptine-QR has been demonstrated to reduce HbA1c by -0.5 to -1.7. The drug has a good safety profile with transient mild to moderate nausea, headache and dizziness as the most frequent adverse events noted with the medication. In a large randomized clinical study of T2DM subjects, bromocriptine-QR exposure was associated with a 42% hazard ratio reduction of a pre-specified adverse cardiovascular endpoint including myocardial infarction, stroke, hospitalization for congestive heart failure, revascularization surgery, or unstable angina. Bromocriptine-QR represents a novel method of treating T2DM that may have benefits for cardiovascular disease as well. ARTICLE HISTORY

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“…The following two arguments do, however, speak against the role of vitamin D deficiency as a trigger of ␤-cell autoimmunity: 1) there is a general recommendation that all young children should take daily vitamin D drops in Northern Europe, and this recommendation is implemented by Ͼ95% of the parents, at least in children up to the age of 2 years; and 2) there are regions with a low type 1 diabetes incidence in Northern Europe, e.g., Russian Karelia, having an annual incidence rate of 7.8/100,000 children under the age of 15 years in the time period of 1990 -1999 compared with a rate of 42 in Finland (32). It has been shown that the mean HbA 1c level varies over the year in children with manifest type 1 diabetes, with the highest values in the fall and winter and with lower levels in the spring and summer (33)(34)(35). This may reflect improved insulin sensitivity in the spring and summer because of more physical exercise.…”

Section: Potential Triggers Of ␤-Cell Autoimmunity and Type 1 Diabetesmentioning

confidence: 99%

Environmental Triggers and Determinants of Type 1 Diabetes

et al. 2005

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Type 1 diabetes is perceived as a chronic immune-mediated disease with a subclinical prodromal period characterized by selective loss of insulin-producing ␤-cells in the pancreatic islets in genetically susceptible subjects. A series of evidence supports a critical role of exogenous factors in the development of type 1 diabetes, such as 1) the fact that <10% of individuals with HLA-conferred diabetes susceptibility do progress to clinical disease, 2) a pairwise concordance of type 1 diabetes of <40% among monozygotic twins, 3) a more than 10-fold difference in the disease incidence among Caucasians living in Europe, 4) a severalfold increase in the incidence over the last 50 years, and 5) migration studies indicating that the disease incidence has increased in population groups who have moved from a low-incidence to a high-incidence region. This article discusses the trigger-booster hypothesis claiming that the diabetic disease process is triggered by an exogenous factor with definite seasonal variation and driven by one or several other environmental determinants. In addition, there are a series of modifying factors affecting the fate and pace of the process. Accordingly, progression to clinical type 1 diabetes typically requires the unfortunate combination of genetic disease susceptibility, a diabetogenic trigger, and a high exposure to a driving antigen. Diabetes 54 (Suppl. 2):S125-S136, 2005

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Seasonal Variation of HbA1c in Intensive Treatment of Children with Type 1 Diabetes

Cited by 33 publications

References 16 publications

Accumulation of severe hypoglycemia at weekends and in warm seasons in patients with type 1 diabetes but not with type 2 diabetes

Accumulation of severe hypoglycemia at weekends and in warm seasons in patients with type 1 diabetes but not with type 2 diabetes

Bromocriptine-QR therapy for the management of type 2 diabetes mellitus: developmental basis and therapeutic profile summary

Environmental Triggers and Determinants of Type 1 Diabetes

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