Glucose intolerance in parkinson's disease

Lipman, Ivan J.; Boykin, Michael E.; Flora, Roger E.

doi:10.1016/0021-9681(74)90031-9

Cited by 59 publications

(43 citation statements)

References 16 publications

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“…The elevated insulin levels in the presence of normal or elevated glucose levels suggests some degree of insulin resistance in the subjects with Rett syndrome. impaired glucose tolerance and elevated insulin levels have been identified in a number of inherited and ac quired neurologic disorders that are characterized by muscle wasting and decreased physical activity, including Friedreich's ataxia [30], Huntington's chorea [31], amyo trophic lateral sclerosis [32], Parkinson's disease [33], and myotonic dystrophy [34], All of these disorders are char acterized by markedly decreased physical activity, which has long been known to cause impaired glucose tolerance [35] , Many arguments have been presented to support the hypothesis that the impaired glucose tolerance in these disorders is not due solely to the decreased activity of the subjects, and there are probably a number of causes for the insulin resistance found in these disorders. The present study did not permit us to determine if our find ings in subjects with Rett syndrome were due to limited physical activity (5 of the 10 subjects were nonambulato ry) or to another abnormality intrinsic to Rett syndrome.…”

Section: Discussionmentioning

confidence: 99%

Abnormalities of Thyroid Function and Glucose Control in Subjects with Rett Syndrome

et al. 1995

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We have identified subtle abnormalities of thyroid function and glucose control in patients with Rett syndrome. The mean serum total thyroxine (T₄) concentration was significantly lower in a group of subjects with Rett syndrome (6.9 ± 1.5 μg/dl, n = 34; p < 0.0001) than the adult reference range (8.5 ± 1.75 μg/dl, n = 200). This difference remained significant even for the 17 subjects not taking anticonvulsants (7.6 ± 1.5 μg/dl; p < 0.05 vs. adult reference). The difference was more marked when compared to age-adjusted normals, with 10 subjects having a serum total T₄ concentration below normal for age including 3 of 17 of the subjects not taking anticonvulsants. This decrease in serum total T₄ concentration was not due to changes in binding proteins as measured by 3,5,3’-triiodothyronine resin uptake, and was associated with a decreased concentration of thyroid-stimulating hormone (1.7 ± 1.6 mU/l, n = 23 vs. 2.5 ± 1.0 mU/l, n = 200; p < 0.01). Oral glucose tolerance tests were performed in 10 of the subjects with Rett syndrome. They had a delay in the peak glucose and insulin concentrations. Glucose levels were elevated at 1 and 2 hours (p < 0.05), and insulin levels were elevated at 1, 2, and 3 hours (p < 0.05). Two subjects fulfilled criteria for impaired glucose tolerance.

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Section: Discussionmentioning

confidence: 99%

Abnormalities of Thyroid Function and Glucose Control in Subjects with Rett Syndrome

et al. 1995

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“…also are frequently associated with a wide variety of neurologic and neuromuscular disorders most of which involve muscle wasting : Parkinson's disease (Boyd et al 1.971;Van Woert and Mueller 1971;Lipman et al 1974; National Diabetes Data Group 1979), Huntington's chorea (Podolsky et al 1972), muscular dystrophy (Dreyfus et al 1954;Danowski et al 1956;Ionaescu and Luca 1963), myotonic dystrophy (Nadler et al 1950;Jacobson et al 1955;Marshall 1959;Caughey and Saucier 1962;Lee and Hughes 1964), chronic peripheral neuropathy (Collis and Engel 1968), late onset proximal myopathy (Collis and Engel 1968), cerebrovascular disease (Jakobson X967;Gertler et al 1972), Friedreich's ataxia (Podolsky et al 1964;Hewer and Robinson 1968;Podolsky and Sheremata 1970;Podolsky 1975), and ataxia telangiectasia (Barlow et al 1965). However, very little is known about glucose metabolism in other forms of spinocerebellar degeneration (SCD).…”

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confidence: 99%

Abnormalities of lipoprotein and carbohydrate metabolism in degenerative diseases of the nervous system - Motor neuron disease and spinocerebellar degeneration.

Murai

Miyahara

Tanaka

et al. 1983

Tohoku J. Exp. Med.

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MURAI, A., MIYAHARA, T., TANAKA, T., KANEKO, T., SAKO, Y. and KAMEYAMA, M. Abnormalities of Lipoprotein and Carbohydrate Metabolism in Degenerative Diseases of the Nervous System -Motor Neuron Disease and Spinocerebellar Degeneration. Tohoku J. exp. Med., 1983, 139 (4), 365-376 The levels of plasma high density lipoprotein (HDL) cholesterol and plasma triglyceride were determined in 44 patients with motor neuron disease (MND) and in 36 patients with spinocerebellar degeneration (SCD). In both groups the HDL cholesterol levels were significantly lower than those in healthy controls, whereas the plasma triglyceride levels were higher than those in the controls. Glucose levels during the oral glucose tolerance test (GTT) were significantly higher in both MND and SCD groups than in healthy controls. Immunoreactive insulin (IRI) levels during GTT were rather higher at 0 and 120 min in both MND and SCD groups than in healthy controls. Glycosylated hemoglobin levels were lower in MND than in the controls. These results indicate that both lipoprotein and carbohydrate metabolisms were impaired in MND and SCD groups. The possibility was presented that denervation might play a part in the pathogenesis of abnormalities of lipoprotein and carbohydrate metabolisms.---motor neuron disease; spinocerebellar degeneration; high density lipoprotein; glucose tolerance test; glycosylated hemoglobin A number of studies have shown a high incidence of impaired glucose metabolism in patients with amyotrophic lateral sclerosis (ALS) (Ionaescu and Luca

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“…Previous epidemiological studies have shown that more than 50% of PD patients exhibit abnormal glucose tolerance or diabetes [32]. Diabetes is estimated to impact 300 million individuals by 2025 [33].…”

Section: Discussionmentioning

confidence: 99%

Methylglyoxal increases dopamine level and leads to oxidative stress in SH-SY5Y cells

Xie¹,

Lin²,

Peng³

et al. 2014

ABBS

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More and more studies have suggested that methylglyoxal (MGO) induced by type-2 diabetes is related to Parkinson's disease (PD). However, little is known about the molecular mechanism. In this study, we explored the MGO toxicity in neuroblastoma SH-SY5Y cells. Neurotoxicity of MGO was measured by mitochondrial membrane potential, malondialdehyde, and methylthiazoletetrazolium assays. The levels of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), and 1-methyl-4-phenyl-1,2,3,4-tetrahydroisoquinoline (salsolinol) were detected by liquid chromatographymass spectrometry/mass spectrometry. The expressions of tyrosine hydroxylase (TH) and dopamine transporter (DAT) were detected by reverse transcriptase polymerase chain reaction and western blot analysis. The results showed that MGO induced an increase in TH and DAT expressions in SH-SY5Y neuroblastoma cells, while the levels of dopamine, DOPAC, and endogenous neurotoxin salsolinol also increased. Aminoguanidine (AG) is an inhibitor of MGO. It was found that AG could decrease the reactive oxygen species (ROS) level induced by MGO, but could not inhibit an increase of TH, DAT and dopamine. The increase of dopamine, DOPAC and salsolinol levels could lead to high ROS and mitochondrial damage. This study suggests that ROS caused by dopamine could contribute to the damage of dopaminergic neurons when MGO is increased during the course of diabetes.

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Glucose intolerance in parkinson's disease

Cited by 59 publications

References 16 publications

Abnormalities of Thyroid Function and Glucose Control in Subjects with Rett Syndrome

Abnormalities of Thyroid Function and Glucose Control in Subjects with Rett Syndrome

Abnormalities of lipoprotein and carbohydrate metabolism in degenerative diseases of the nervous system - Motor neuron disease and spinocerebellar degeneration.

Methylglyoxal increases dopamine level and leads to oxidative stress in SH-SY5Y cells

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