[Primary evaluation of the behaviour eating disorder in obese and type 2 diabetic Algerian subjects]. / Evaluation primaire des troubles du comportement alimentaire chez le sujet obèse et le patient diabétique de type 2 algérien.

BACKGROUND: Glucose imbalance in type 2 diabetes and massive weight gain in obese subjects are disorders that are correlated with Behaviour Eating Disorder (BED), leading to a hypercaloric, sweet and fat oriented diet. AIM: This study examined how BED such as dietary restriction, disinhibition, and hunger, are assessed by Three Factor Eating Questionnaire (TFEQ) and Dutch Eating Behaviour Questionnaire (DEBQ). METHODS: In the present investigation these factors were studied in a sample of Algerian population composed of 30 obese subjects, 70 type 2 diabetic patients and 30 healthy subjects. 51 questions or items were used for the TFEQ test and 33 questions for the DEBQ test. RESULTS: Multivariate analysis showed that restriction and disinhibition were significantly associated with obesity and diabetes pathogenesis. Compared to healthy subjects, obese patients showed a significant hyperphagic BED type (disinhibition and hunger disorders). These BED are associated with psycho-sensory disorders as characterized by externality and emotivity. Conversely, the diabetic patient showed both hypophagic and hyperphagic BED. CONCLUSION: In this study, the role of BED in obesity genesis and in glycaemia dysregulation of the diabetes pathology seems to be confirmed. An early identification of these disorders deserves further investigation in a broad Algerian population in order to treat them.

[Metabolic syndrome and hormonal interaction in obese and type 2 diabetic Algerian subject: the behavior eating disorder impact]. / Syndrome métabolique et interaction hormonale chez le sujet obèse et le patient diabétique de type 2 algérien: impact des troubles du comportement alimentaire.

BACKGROUND: These twenty last years, the metabolic syndrome was accused in various human pathologies including android obesity and type 2 diabetes. In obesity, increased body weight is frequently associated with excessive caloric food and sedentary activities. The Behaviour Eating Disorders (BED) is involved in over-consumption alimentary. In Algeria, we observed increasingly deviations in life-style alimentary, from the Mediterranean-Cretan model to American fast-food model. AIM: To study interactions between the BED, hormonal secretions and metabolic syndrome parameters. METHODS: The present study was undertaken on Algerian population cohorts composed of 30 obese subjects, 70 type 2 diabetic patients and 30 healthy subjects. The BED was evaluated by TFEQ and DEBQ tests. Anthropometric parameters (waist circumference, IMC), metabolic parameters (glucose, triglycerides, HDL-C, LDL-C) and hormones (insulin, peptide C, ACTH, cortisol, GH) were determinates by biometrics, spectrophotometry and radioimmunology methods, respectively. RESULTS: Multivariate analyses showed the high correlation between the BED and the metabolic syndrome, particularly a critical insulinoresistance state (IR). This IR generates in periphery a whole of metabolic disorders: dyslipidemia, hyperglycemia and hypertrophy of adipose tissue. In diabetic and obese patients, cortisol, ACTH and GH secretions are insidiously altered and to lead metabolic disorders. CONCLUSION: In this study, the role of the BED in obesity and diabetes genesis seems to be confirmed. In response to nutritional stress, the BED generates a hyperactivity of endocrine pancreas, adrenal gland, and pituitary gland. It appeared that Algerian population is not adapted to fast-food American model.

Low rate of glucose 6-phosphate hydrolysis in liver cells is a physiological feature of non-diabetic wild sand rats (Psammomys obesus).

OBJECTIVE: In this study we have compared glucose metabolism and liver gluconeogenesis in wild adult desert gerbil Psammomys obesus fed with their natural halophilic plants and Wistar rats fed on a laboratory chow. Psammomys obesus is a natural model of insulin resistance when fed a rodent laboratory chow. METHODS: Basal glucose and insulin were determined in plasma of fasting animals. Hepatocyte gluconeogenesis from lactate-plus-pyruvate was investigated in perifused hepatocytes by assessing simultaneously glucose synthesis rate and intracellular oxaloacetate, phosphoenolpyruvate, 3-phosphoglycerate, fructose 6-phosphate and glucose 6-phosphate (G6P) under true steady state conditions. RESULTS: Fasting blood glucose (2.8 +/- 0.1 vs 4.8 +/- 0.4 mmol.L(- 1)) and plasma insulin concentration (129 +/- 14 vs 150 +/- 21 pmol.L(-1)) were significantly lower in Psammomys as compared to albino rats. Maximal gluconeogenic rate was also lower in Psammomys (2.3 +/- 0.3 vs 5.1 +/- 0.3 micromol x min(-1) x g dry cells(-1)). This effect was related to a slower hydrolysis of G6P. CONCLUSION: A lower G6P hydrolysis in Psammomys as compared to wistar was the main difference between the two groups of liver cells. Such feature may represent the major metabolic adaptation permitting Psammomys to survive despite its severe restrictive natural conditions. Indeed, a low G6P hydrolysis allows an insulin resistance state, with a high lipogenic activity, but associated with low blood glucose. The rise in blood glucose occurring when Psammomys are fed with exogenous carbohydrates perturbs such delicate metabolic equilibrium, resulting thus in a diabetic state because of the deleterious effect of hyperglycemia.

Mitochondrial metabolism and type-2 diabetes: a specific target of metformin.

Several links relate mitochondrial metabolism and type 2 diabetes or chronic hyperglycaemia. Among them, ATP synthesis by oxidative phosphorylation and cellular energy metabolism (ATP/ADP ratio), redox status and reactive oxygen species (ROS) production, membrane potential and substrate transport across the mitochondrial membrane are involved at various steps of the very complex network of glucose metabolism. Recently, the following findings (1) mitochondrial ROS production is central in the signalling pathway of harmful effects of hyperglycaemia, (2) AMPK activation is a major regulator of both glucose and lipid metabolism connected with cellular energy status, (3) hyperglycaemia by inhibiting glucose-6-phosphate dehydrogenase (G6PDH) by a cAMP mechanism plays a crucial role in NADPH/NADP ratio and thus in the pro-oxidant/anti-oxidant cellular status, have deeply changed our view of diabetes and related complications. It has been reported that metformin has many different cellular effects according to the experimental models and/or conditions. However, recent important findings may explain its unique efficacy in the treatment of hyperglycaemia- or insulin-resistance related complications. Metformin is a mild inhibitor of respiratory chain complex 1; it activates AMPK in several models, apparently independently of changes in the AMP-to-ATP ratio; it activates G6PDH in a model of high-fat related insulin resistance; and it has antioxidant properties by a mechanism (s), which is (are) not completely elucidated as yet. Although it is clear that metformin has non-mitochondrial effects, since it affects erythrocyte metabolism, the mitochondrial effects of metformin are probably crucial in explaining the various properties of this drug.