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A mutation of mitochondrial DNA may be associated with both insulin-dependent diabetes (IDDM) and non-insulin-dependent diabetes (NIDDM). Mitochondrial DNA is the genetic material associated with the energy-producing compartments of cells. Researchers in Japan identified a particular mitochondrial DNA mutation in three of 55 (6%) patients with IDDM and a history of diabetes in first-degree relatives, in two of 100 (2%) patients with NIDDM and a history of diabetes in first-degree relatives, in three of five (60%) patients with diabetes and hearing loss and in eight of 39 (21%) patients with a syndrome consisting of mitochondrial muscle disease, degenerative brain disease, accumulation of lactic acid and stroke-like episodes. The mutation was also found in 62 relatives of the patients studied. The mutation was not found in 85 patients with IDDM who had no family history of diabetes or in 200 healthy persons with no family history of diabetes. The mutation may cause some cases of both IDDM and NIDDM in Japan, and it appears to be inherited from a mother with diabetes.

The biological role of peroxisome proliferator-activated receptor γ (PPARγ) was investigated by gene targeting and case±control study of the Pro12Ala PPARγ2 polymorphism. Homozygous PPARγ-deficient embryos died at 10.5–11.5 days post conception (dpc) due to placental dysfunction. Heterozygous PPARγ-deficient mice were protected from the development of insulin resistance due to adipocyte hypertrophy under a high-fat diet, whose phenotypes were abrogated by PPARγ agonist treatment. Heterozygous PPARγ-deficient mice showed over-expression and hypersecretion of leptin despite the smaller size of adipocytes and decreased fat mass, which may explain these phenotypes at least in part. This study reveals a hitherto unpredicted role for PPARγ in high-fat diet-induced obesity due to adipocyte hypertrophy and insulin resistance, which requires both alleles of PPARγ. A Pro12Ala polymorphism has been detected in the human PPARγ2 gene. Since this amino acid substitution may cause a reduction in the transcriptional activity of PPARγ, this polymorphism may be associated with decreased insulin resistance and decreased risk of type 2 diabetes. To investigate this hypothesis, we performed a case±control study of the Pro12Ala PPARγ2 polymorphism. In an obese group, subjects with Ala12 were more insulin sensitive than those without. The frequency of Ala12 was significantly lower in the diabetic group, suggesting that this polymorphism protects against type 2 diabetes. These results revealed that in both mice and humans, PPARg is a thrifty gene mediating type 2 diabetes. [ABSTRACT FROM PUBLISHER]

Diet treatment for diabetes requires restriction of the food amount (energy intake). It is desirable that patients have a proper relative consumption of the three main nutrients (proteins, carbohydrates, fats) and also habitually take low-energy foods such as vegetables, mushrooms and seaweeds, etc. as often as possible in each meal. Therefore, we can replace the expression ‘a diet for diabetes’ with ‘a diet for healthy living’. By showing a clinical case of an obese diabetic patient, who succeeded to reduce their body weight, HbA1c and oral agents through diettreatment, and finally could go on diet treatment only, the importance of diet therapy can be emphasized. Furthermore, the estimation index was examined to evaluate how accurately diabetic patients could estimate food energy. According to this study, a large amount of food on the plate leads most patients to underestimate the amount of real energy, and patients are apt to eat too much compared with having smaller amounts of food on the plate. By analyzing questionnaires on the diet therapy of approximately 3000 diabetics, it has been shown that the majority of patients at our hospital recognize that diet therapy is the most important factor in the treatment of diabetes. Interestingly, patients who ate all the food served showed a significantly higher body mass index compared with those who left served food. [ABSTRACT FROM PUBLISHER]