A cross-sectional study for glucose intolerance of myotonic dystrophy

Matsumura, Tsuyoshi; Iwahashi, Hiromi; Funahashi, Tohru; Takahashi, Masanori; Saito, Tomoko; Yasui, Kumiko; Saitô, Toshio; Iyama, Akinori; Toyooka, Keiko; Fujimura, Harutoshi; Shinno, Susumu

doi:10.1016/j.jns.2008.08.037

Cited by 33 publications

(42 citation statements)

References 40 publications

(46 reference statements)

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“…Our results are consistent with the report of Matsumura et al (15) who showed that that ACRP30 concentrations were lower in patients with glucose concentrations comparable to those of our patients (i.e. between 90 and 110 mg/dl).…”

Section: Discussionsupporting

confidence: 93%

“…To date, only two studies have evaluated ACRP30 expression in DM1 patients (15,16), although DM1 is considered a good model for the study of metabolic perturbations in IR with adequate islet compensation. To determine whether the metabolic perturbations in DMI are associated with deranged adiponectin expression, we measured circulating levels of ACRP30 and characterized its oligomerization pattern.…”

Section: Introductionmentioning

confidence: 99%

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Decreased concentration of adiponectin together with a selective reduction of its high molecular weight oligomers is involved in metabolic complications of myotonic dystrophy type 1

Daniele

Rosa

Cristofaro

et al. 2011

European Journal of Endocrinology

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Objective: The hormone adiponectin exerts beneficial pleiotropic effects on biological and metabolic processes. Although a well-recognized insulin sensitizer, its characteristic has yet to be clearly defined. Myotonic dystrophy type 1 (DM1) is a rare genetic disorder that features muscle wasting and metabolic comorbidity, and patients have an increased risk of developing type 2 diabetes. We analyzed circulating levels of adiponectin and its oligomers to determine whether their expression correlates with metabolic alterations in DM1 patients. Design and methods: We measured the anthropometric and biochemical features and three insulin resistance (IR) indices (homeostasis model assessment, quantitative insulin sensitivity check index, and McAuley) of 21 DM1 patients and of 82 age-, sex-, and weight-matched controls. In the blood samples of patients and controls, adiponectin levels were measured by ELISA, and its oligomers were characterized by using western blotting and gel filtration. The adiponectin gene was molecularly analyzed in patients. Results: DM1 patients had significantly higher body mass index, waist circumference, triglycerides (TGs), glucose, tumor necrosis factor a, and IR; conversely, they had significantly lower concentrations of total serum adiponectin with a selective, pronounced decrease of its high molecular weight (HMW) oligomers. There was a strong negative correlation between adiponectin and TGs in DM1 patients. Conclusions: Our results endorse the hypothesis that decreased expression of adiponectin together with a selective reduction of its HMW oligomers contributes to the worsening of IR and its metabolic complications in DM1 patients. These findings suggest that adiponectin and HMW oligomers may serve as biomarkers and are promising therapeutic agents for IR and its consequences in DM1.European Journal of Endocrinology 165 969-975

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Decreased concentration of adiponectin together with a selective reduction of its high molecular weight oligomers is involved in metabolic complications of myotonic dystrophy type 1

Daniele

Rosa

Cristofaro

et al. 2011

European Journal of Endocrinology

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“…In fact, it is reported that insulin sensitivity in skeletal muscle is decreased by 70% in patients with DM1 [3], while whole body glucose disposal is reduced by 15-25% following insulin infusion [4]. Due to focal insulin resistance in muscle, the incidence of diabetes is only 5-9% in these patients [5]. However, since the obesity induces insulin resistance in adipose tissue and liver in addition to skeletal muscle, glucose intolerance may be more severe in overweight patients with DM1.…”

mentioning

confidence: 99%

“…While serum adiponectin level are low in the patients with type 2 diabetes, it has been shown that TZDs increase circulating adiponectin level in diabetic subjects, probably by activating peroxisome proliferator-activated receptors (PPARs) [8]. Unexpectedly, it was reported that newly diagnosed patients with DM1 have high adiponectin levels compared with general control [5]. This finding may be due to the compensatory reaction for deterioration of insulin sensitivity in non-obese subjects with mild glucose intolerance.…”

mentioning

confidence: 99%

Dramatic Improvement of Blood Glucose Control after Pioglitazone Treatment in Poorly Controlled Over-weight Diabetic Patients with Myotonic Dystrophy

et al. 2009

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itself is a positive modulator of insulin action in muscle [2]. These findings support the presence of insulin resistance specifically in DM1 skeletal muscle in patients with DM1. In fact, it is reported that insulin sensitivity in skeletal muscle is decreased by 70% in patients with DM1 [3], while whole body glucose disposal is reduced by 15-25% following insulin infusion [4]. Due to focal insulin resistance in muscle, the incidence of diabetes is only 5-9% in these patients [5]. However, since the obesity induces insulin resistance in adipose tissue and liver in addition to skeletal muscle, glucose intolerance may be more severe in overweight patients with DM1.Thiazolidinediones (TZDs) are effective in the treatment of diabetes associated with insulin resistance. A few reports show its usefulness in the management of insulin resistance in skeletal muscle in Abstract. Insulin resistance is mainly present in skeletal muscle in non-obese patients with myotonic dystrophy. Thiazolidinediones are reported to reduce insulin resistance in these patients. However, the effects of pioglitazone in overweight patients with myotonic dystrophy and type 2 diabetes mellitus have not been established. Here, we evaluated the effect of pioglitazone in two poorly-controlled over-weight diabetic patients with myotonic dystrophy. Case 1 was a 41-year-old women (BMi 27.8 kg/m 2 ) with myotonic dystrophy and type 2 diabetes had been treated with 3 mg/day glimepiride and 500 mg/day metformin, but the treatment failed to achieve good glycemic control (HbA 1C 11.8 %). Following admission to the hospital, she was treated with low-dose insulin and 30 mg/day pioglitazone. At 10 days after initiation of therapy, glycemic control was improved, serum iL-6 and hs-CRP decreased, and adiponectin level increased rapidly. Case 2 was a 47-year-old women (BMi 29.2kg/m 2 ) with myotonic dystrophy and type2 diabetes mellitus had been treated with insulin without successful glycemic control (HbA 1C 10.3 %). After admission, she was treated with 15 mg/day pioglitazone. This improved glycemic control, reduced daily insulin requirement, decreased iL-6 and hs-CRP levels rapidly and increased adiponectin level at 10 days after initiation of therapy. in both cases, pioglitazone rapidly improved glycemic control, enhanced adiponectin production, and reduced inflammatory cytokines. These results suggest that pioglitazone may be suitable for these patients.

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“…Other ocular defects include decreased vision and decreased intraocular pressure (Rosa et al, 2011). Patients with DM1 could also present endocrine defects including insulin resistance and gonadal atrophy (García de Andoin et al, 2005;Matsumura et al, 2009), as well as smooth muscle dysfunction, the clinical effects of which are observed mainly in the gastrointestinal tract and result in disordered esophageal and gastric peristalsis (Machuca-Tzili L et al, 2005).…”

Section: Multisystemic Symptomatologymentioning

confidence: 99%