Marieke van Dijk

Leiden University Medical Centre, Leyden, South Holland, Netherlands

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Publications (8)32.35 Total impact

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    ABSTRACT: Type 1 diabetes mellitus wordt gekenmerkt door een absoluut tekort aan insuline. Uit eerdere onderzoeken is echter gebleken dat insulineresistentie ook voorkomt bij patiënten met type 1 diabetes mellitus. Welke mechanismen ten grondslag liggen aan het ontstaan van insulineresistentie bij type 1 diabetes mellitus is onvoldoende bekend.
    No preview · Article · Dec 2015
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    ABSTRACT: We have previously shown that acute sleep curtailment induces insulin resistance, both in healthy individuals as well as in patients with type 1 diabetes, suggesting a causal role for sleep disturbances in pathogenesis of insulin resistance, independent of endogenous insulin production. However, the underlying mechanisms remain unclear. This study aimed to explore the metabolic pathways affected by sleep loss using targeted metabolomics in human fasting plasma samples. Healthy individuals (n = 9) and patients with type 1 diabetes (n = 7) were studied after a single night of short sleep (4 hours) versus normal sleep (8 hours) in a cross-over design. Strikingly, one night of short sleep specifically increased the plasma levels of acylcarnitines, essential intermediates in mitochondrial fatty acid oxidation (FAO). Specifically, short sleep increased plasma levels of tetradecenoyl-L-carnitine (C14:1) (+32%, p=2.67*10(-4)), octadecanoyl-L-carnitine (C18:1) (+22%, p=1.92*10(-4)) and octadecadienyl-L-carnitine (C18:2) (+27%, p=1.32*10(-4)). Since increased plasma acylcarnitine levels could be a sign of disturbed FAO, it is possible that sleep curtailment acutely induces inefficient mitochondrial function. Our observations provide a basis for further research into the role of acylcarnitines as a potential mechanistic pathway by which sleep deprivation - even short term - causes adverse metabolic effects, such as insulin resistance.
    Full-text · Article · Sep 2015 · Archives of Biochemistry and Biophysics
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    ABSTRACT: Previous studies have indicated that women with diabetes mellitus are at higher risk to develop sexual dysfunctions. In the current study, we hypothesized that lower genital arousal response-as a consequence of diabetes-related damage to nerves and blood vessels-might play a part in these higher prevalence rates. Vaginal blood flow, subjective sexual response, and clitoral sensitivity were compared between women with diabetes and healthy controls, and associations with diabetes complications were investigated. In pre- and postmenopausal women with type 1 diabetes (n = 42) and healthy controls (n = 46), vaginal blood flow was measured as vaginal pulse amplitude (VPA). VPA was assessed at rest, during erotic film viewing, and during vibrotactile clitoral stimulation. Subjective sexual arousal was measured using a questionnaire. Clitoral sensitivity was assessed by a vibration perception test. Data on diabetes complications were obtained from medical records, and neuropathy was assessed by quantitative sensory testing. VPA, subjective sexual arousal, and clitoral sensitivity were not significantly different between women with diabetes and controls. Nevertheless, women with diabetes who had retinopathy showed significantly lower VPA than women without retinopathy, and women with diabetes who had neuropathy showed significantly higher sensation thresholds for vibrotactile clitoral stimulation. The results do not support the hypothesis of a disrupted genital arousal response in women with diabetes. However, the observed associations between retinopathy and vaginal blood flow, and between neuropathy and clitoral sensitivity, suggest that diabetes-related complications might adversely affect the physiological basis of female sexual response.
    Full-text · Article · Jun 2015 · Archives of Sexual Behavior
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    ABSTRACT: Objective: Patients treated for nonfunctioning pituitary macroadenomas (NFMAs) have fatigue and alterations in sleep characteristics and sleep-wake rhythmicity frequently. As NFMAs often compress the optic chiasm, these complaints might be related to dysfunction of the adjacent suprachiasmatic nucleus (SCN). We aimed to explore whether indirect indices of SCN functioning are altered in the long term after surgery for NFMAs. Methods: We studied 17 NFMA patients in long-term remission after transsphenoidal surgery, receiving adequate and stable hormone replacement for hypopituitarism, and 17 control subjects matched for age, gender, and BMI. Indirect indices of SCN function were assessed from 24-h ambulatory recordings of skin and core body temperatures, blood pressure, and salivary melatonin levels. Altered melatonin secretion was defined as an absence of evening rise, considerable irregularity, or daytime values >3 pg/ml. We additionally studied eight patients treated for craniopharyngioma. Results: Distal-proximal skin temperature gradient did not differ between NFMAs and control subjects, but proximal skin temperature was decreased during daytime (P=0.006). Core body temperature and non-dipping of blood pressure did not differ, whereas melatonin secretion was often altered in NFMAs (OR 5.3, 95% CI 0.9-30.6). One or more abnormal parameters (≥2.0 SDS of control subjects) were observed during nighttime in 12 NFMA patients and during daytime in seven NFMA patients. Similar patterns were observed in craniopharyngioma patients. Conclusion: Heterogeneous patterns of altered diurnal rhythmicity in skin temperature and melatonin secretion parameters were observed in the majority of patients treated for NFMAs. On a group level, both NFMA and craniopharyngioma patients showed a lower daytime proximal skin temperature than control subjects, but other group averages were not significantly different. The observations suggest altered function of central (or peripheral) clock machinery, possibly by disturbed entrainment or damage of the hypothalamic SCN by the suprasellar macroadenoma or its treatment.
    Full-text · Article · May 2014 · European Journal of Endocrinology
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    ABSTRACT: Patients with type 1 diabetes have altered sleep characteristics and are thought to have deficits in sustained attention. We compared the Sustained Attention to Response Task (SART) of patients with type 1 diabetes to that of healthy controls, and related results with sleep characteristics and disease- related factors. The SART was applied in 122 patients and 109 controls. Glucoregulation was assessed by HbA1c -values and a questionnaire assessing glycaemic history. Clinical parameters were obtained from medical charts. Polyneuropathy was assessed by neurological examination and quantitative sensory testing. Sleep characteristics were assessed with sleep questionnaires. Anxiety and depression scores were assessed by the Hospital Anxiety and Depression Scale (HADS). The SART reaction time (RT) was significant longer than in controls (327 ± 5 ms vs. 285 ± 3 ms, p < 0.001), although there were no significant differences in error scores. Repeated measurement analyses showed that diabetes per se was associated with prolonged RT (P < 0.001). None of the sleep-related and diabetes-related factors were associated with SART parameters. Patients with type 1 diabetes had prolonged RT as evidence of impaired sustained attention, which was associated with diabetes per se, but not with disturbed sleep characteristics. This article is protected by copyright. All rights reserved.
    No preview · Article · Sep 2013 · Diabetes/Metabolism Research and Reviews
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    ABSTRACT: Background: The aim of this study was to determine whether insulin resistance is present in lean patients with uncomplicated type 1 diabetes mellitus on long-term continuous subcutaneous insulin infusion (CSII), compared with matched healthy controls. Methods: We studied eight patients (four men and four women) with type 1 diabetes mellitus on continuous subcutaneous insulin infusion and eight healthy controls, matched for age, gender and body mass index. Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp studies with infusion of [6,6-(2) H(2)] glucose. Results: Endogenous glucose production did not differ in the basal state between patients and controls. However, endogenous glucose production was less suppressed during clamp conditions in patients compared with controls (64% vs 79%, p = 0.01), indicating decreased hepatic insulin sensitivity. During the clamp study, glucose disposal rate was ~38% lower in patients compared with controls (24.4 ± 2.5 vs 39.7 ± 5.6 µmol/kgLBM/min, p = 0.04). Accordingly, the rate of infusion of glucose was ~51% lower in patients (17.7 ± 2.8 vs 39.7 ± 5.7 µmol/kgLBM/min, p = 0.02). Finally, non-esterified fatty acids levels were ~2.5 times higher in patients during steady state clamp conditions (150 ± 26 vs 58 ± 4 pmol/L, p = 0.01), reflecting decreased insulin sensitivity of lipolysis. Conclusions: Insulin resistance is a prominent feature of lean patients with type 1 diabetes mellitus, despite long term and stable treatment with continuous subcutaneous insulin infusion. Insulin resistance in type 1 diabetes involves both lipolysis, hepatic and peripheral glucose metabolism.
    No preview · Article · Jan 2013 · Diabetes/Metabolism Research and Reviews
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    ABSTRACT: Subsequent nights with partial sleep restriction result in impaired glucose tolerance, but the effects on insulin sensitivity have not been characterized. The aim of this study was to evaluate the effect of a single night of partial sleep restriction on parameters of insulin sensitivity. Nine healthy subjects (five men, four women) were studied once after a night of normal sleep duration (sleep allowed from 2300 to 0730 h), and once after a night of 4 h of sleep (sleep allowed from 0100 to 0500 h). Sleep characteristics were assessed by polysomnography. Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp studies (from 1130 to 1430 h) with infusion of [6,6-(2)H(2)]glucose. Sleep duration was shorter in the night with sleep restriction than in the unrestricted night (226 +/- 11 vs. 454 +/- 9 min; P< 0.0001). Sleep restriction did not affect basal levels of glucose, nonesterified fatty acids, insulin, or endogenous glucose production. Sleep restriction resulted in increased endogenous glucose production during the hyperinsulinemic clamp study compared to the unrestricted night (4.4 +/- 0.3 vs. 3.6 +/- 0.2 micromol x kg lean body mass(-1) x min(-1); P = 0.017), indicating hepatic insulin resistance. In addition, sleep restriction decreased the glucose disposal rate during the clamp (32.5 +/- 3.6 vs. 40.7 +/- 5.1 micromol x kg lean body mass(-1) x min(-1); P = 0009), reflecting decreased peripheral insulin sensitivity. Accordingly, sleep restriction decreased the rate of glucose infusion by approximately 25% (P = 0.001). Sleep restriction increased plasma nonesterified fatty acid levels during the clamp study (68 +/- 5 vs. 57 +/- 4 micromol/liter; P = 0.005). Partial sleep deprivation during only a single night induces insulin resistance in multiple metabolic pathways in healthy subjects. This physiological observation may be of relevance for variations in glucoregulation in patients with type 1 and type 2 diabetes.
    Full-text · Article · Apr 2010 · The Journal of Clinical Endocrinology and Metabolism
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    ABSTRACT: Sleep restriction results in decreased insulin sensitivity and glucose tolerance in healthy subjects. We hypothesized that sleep duration is also a determinant of insulin sensitivity in patients with type 1 diabetes. We studied seven patients (three men, four women) with type 1 diabetes: mean age 44 +/- 7 years, BMI 23.5 +/- 0.9 kg/m(2), and A1C 7.6 +/- 0.3%. They were studied once after a night of normal sleep duration and once after a night of only 4 h of sleep. Sleep characteristics were assessed by polysomnography. Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp studies with an infusion of [6,6-(2)H(2)]glucose. RESULTS Sleep duration was shorter in the night with sleep restriction than in the unrestricted night (469 +/- 8.5 vs. 222 +/- 7.1 min, P = 0.02). Sleep restriction did not affect basal levels of glucose, nonesterified fatty acids (NEFAs), or endogenous glucose production. Endogenous glucose production during the hyperinsulinemic clamp was not altered during the night of sleep restriction compared with the night of unrestricted sleep (6.2 +/- 0.8 vs. 6.9 +/- 0.6 micromol x kg lean body mass(-1) x min(-1), NS). In contrast, sleep restriction decreased the glucose disposal rate during the clamp (25.5 +/- 2.6 vs. 22.0 +/- 2.1 micromol x kg lean body mass(-1) x min(-1), P = 0.04), reflecting decreased peripheral insulin sensitivity. Accordingly, sleep restriction decreased the rate of glucose infusion by approximately 21% (P = 0.04). Sleep restriction did not alter plasma NEFA levels during the clamp (143 +/- 29 vs. 133 +/- 29 micromol/l, NS). Partial sleep deprivation during a single night induces peripheral insulin resistance in these seven patients with type 1 diabetes. Therefore, sleep duration is a determinant of insulin sensitivity in patients with type 1 diabetes.
    Full-text · Article · Mar 2010 · Diabetes care