By its action in the central nervous system (CNS), insulin contributes in the regulation of lifespan, neuronal survival, feeding behaviour, energy balance, glucose and fat metabolism, reproduction and cognition. The pleiotropic central action of insulin is under a multilevel control via metabolic, endocrine and neural signals. Of particular interest is the interaction of insulin in the hypothalamus with anabolic and catabolic peptides and neurotransmitters. Insulin shares common signalling pathways involved in energy and glucose homeostasis and dialogues with numerous neuroregulators, in particular the anorexigenic peptide leptin and the neurotransmitter serotonin.
A new concept on the onset of metabolic pathologies highlights the importance of an efficient central insulin action in animals and humans and, states that the combination of defective pancreatic beta-cell function and insulin resistance not only in classical, peripheral, insulin target tissues but in every tissue contributes to the onset of the diseases. Impaired brain insulin signalling is a link coupling obesity to diabetes. This impairment may be related to either genetic factors, and/or environmental factors such as diminished physical activity, stress, over or/and inappropriate nutrition. Insulin, leptin and serotonin, are also involved in comorbidities linked to metabolic diseases, such as depression and Alzheimer's disease.
Current approaches used for the prevention and treatment of type 2 diabetes are not adequately effective. Most of the antidiabetic therapies induce many adverse effects, in particular obesity, and thus may initiate a vicious cycle of problems. In order to develop novel, more efficient, ways of prevention and intervention strategies for metabolic pathologies, there is an urgent need for a better understanding of insulin action in the brain and of the cross-talk of central and peripheral mechanisms. At present, new routes of drug administration targeting insulin and its partners in the CNS, resulting in increased central efficiency of the hormone, offer hope for improved antidiabetic action with diminished side effects.

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Glycated hemoglobin (HbA₁c) is decreased by iron treatment in patients with iron deficiency anemia (IDA). We studied HbA₁c and glycated albumin (GA) in 4 diabetic patients with IDA—2 men and 2 women aged 58.3±14.5 years old with a body mass index (BMI) of 24.1±4.0 kg/m². We administered sodium ferrous citrate (100 mg/day) for 4-8 weeks to raise hemoglobin (Hb) and serum ferritin to normal levels. Twelve weeks after iron treatment, Hb had improved from 9.5±1.0 g/dl to 12.8±1.0 g/dl and mean corpuscular hemoglobin (MCH) from 23.4±1.0 pg to 30.3±0.9 pg. HbA₁c decreased from 7.9±0.6% before treatment to 6.3±0.3% 4 weeks after treatment, gradually increasing to 7.7±1.0% at 12 weeks. Mean serum GA did not change significantly during and after iron treatment, indicating that serum GA is a more suitable marker rather than HbA₁c for glycemic control, after iron treatment in diabetic patients with IDA.

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[in Japanese]

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[in Japanese]

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