Abstract
The 3243 A>G mutation in mitochondrial DNA is the most common cause of monogenic diabetes mellitus in Japan. A 45-year-old woman with mitochondrial diabetes and significant insulin resistance presented with hypoadiponectinemia despite a normal amount of visceral fat. Three months of treatment with pioglitazone (PIO) improved her blood glucose profile and response to the 75-g oral glucose tolerance test. These changes were accompanied by the amelioration of her insulin resistance and the impairment of early-phase insulin secretion. Her serum adiponectin levels increased to the normal range. In this case of mitochondrial diabetes, PIO was effective for glycemic control.
MeSH terms
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Adiponectin / blood
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Adiponectin / deficiency
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Blood Glucose / metabolism
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DNA, Mitochondrial / genetics
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Diabetes Mellitus, Type 2 / blood
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Diabetes Mellitus, Type 2 / drug therapy*
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Diabetes Mellitus, Type 2 / genetics
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Female
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Glucose Tolerance Test
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Humans
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Hypoglycemic Agents / therapeutic use*
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Insulin / blood
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Insulin Resistance / physiology
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Metabolism, Inborn Errors / drug therapy
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Metabolism, Inborn Errors / etiology
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Middle Aged
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Mitochondria / drug effects
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PPAR gamma / agonists*
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Pedigree
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Pioglitazone
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Thiazolidinediones / therapeutic use*
Substances
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ADIPOQ protein, human
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Adiponectin
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Blood Glucose
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DNA, Mitochondrial
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Hypoglycemic Agents
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Insulin
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PPAR gamma
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Thiazolidinediones
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Pioglitazone