Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
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Exp. Clin. Endocrinol. Diabetes · Jan 1998
ReviewTo be lean or not to be lean. Is leptin the answer?
Leptin and the leptin receptor genes have been identified as the site of mutations in the peripheral adipocyte hormone pathway responsible for obesity in the ob/ob mouse (Zhang et al., 1994) and the db/db mouse (Chen et al., 1996). In obese humans, ob/ob like mutations in leptin are rare but confirm a role for leptin (Montague et al., 1997), and db/db like mutations in the leptin receptor have not been found (Considine et al., 1996a); however, the increased understanding of the molecular basis for obesity has generated tremendous interest among scientists and patients alike. The new knowledge could be the base for intelligent drugs for the treatment of obesity. Herein we will put in perspective a) the physiological background that led to the discovery of leptin, b) leptin biosynthesis, c) leptin action and d) the clinical issues related to leptin as a drug for the treatment of obesity.
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Exp. Clin. Endocrinol. Diabetes · Jan 1998
Influence of metabolic control and duration of disease on microvascular dysfunction in diabetes assessed by laser Doppler anemometry.
A reduced and delayed postocclusive reactive hyperaemia has been demonstrated in diabetic patients using videophotometric capillaroscopy and laser Doppler fluxmetry. The aim of the present study was to examine by means of the new technique of laser Doppler anemometry whether impairment of skin microcirculation differs between type 1 and type 2 diabetic patients especially with regard to metabolic control and duration of diabetes. Sixteen type 1 and 19 type 2 diabetic patients were investigated and subdivided in patients with "good" (HbA1c < 7.5%) or "bad" (HbA1c > 7.5%) metabolic control and in patients with a diabetes duration of less or more than 10 years. ⋯ In type 2 diabetes time to peak CBV (46.8 +/- 8.5 s vs. 16.4 +/- 2.2 s, p < 0.001) was also prolonged already in the first 10 years of the disease. However with regard to metabolic control a reduced peak CBV (0.54 +/- 0.04 mm/ s vs. 0.70 +/- 0.04 mm/s, p < 0.05) and a prolonged time to peak CBV (56.6 +/- 14.8 s vs. 13.7 +/- 2.7 s, p < 0.01) was found in type 2 diabetes only in the group of patients with HbA1c > 7.5%. The results indicate that in type 2 diabetes actual metabolic control might be of greater importance for the microvascular dysfunction than in type 1 diabetes and that the skin capillary circulation is impaired already in the first 10 years of both diabetes types.