Influence of the urban context on the relationship between neighbourhood deprivation and obesity.

BACKGROUND: In middle- and high-income countries, obesity is positively associated with neighbourhood deprivation. However, the moderating effect of the broader urban residential context on this relationship remains poorly understood. METHODS: In this study, we have examined the nonlinear and geographically varying relationship between neighbourhood deprivation and the likelihood of being a person with overweight among participants of the French NutriNet-Santé adult cohort study (n = 68,698), adjusted for age, gender and educational level. Ten urban residential contexts (e.g., suburbs, peri-urban or rural areas) were defined. We used a multilevel generalised additive modelling framework for analyses. RESULTS: We found that the relationship between neighbourhood deprivation and overweight differed according to urban context, in terms of both linearity and intensity. Overall, the deprivation-overweight relationship was strongly positive (with a higher prevalence of overweight in deprived neighbourhoods) in suburban areas of Paris and of other large French cities, while weak or null in small towns and rural areas, and intermediate in inner cities. In addition, we observed in suburbs of Paris and in peri-urban belts of large cities that beyond a certain level of neighbourhood deprivation, the relationship with overweight plateaued. DISCUSSION: In a French population from a high-income country, suburbs, as well as moderately deprived neighbourhoods of peri-urban areas of large cities, are potential targets for public health and urban planning policies aiming at preventing obesity. Our results emphasize the value of local analyses to better capture the complexity and contextual variations of socioeconomic determinants of non-communicable diseases such as obesity.

Effects of chronic administration of sodium 2 chloropropionate in normal and diabetic dogs.

Pancreatic hormonal and metabolic responses to chronic administration of sodium 2 chloropropionate (2 CP) were investigated in conscious dogs. We subcutaneously administered 2 CP daily for 7 days at the dose of 0.58 mmol/kg (62.5 mg/kg) in normal dogs and those rendered diabetic by injection of alloxan (0.24 mmol/kg, i.v.). In the normal dogs, the chronic administration of 2 CP provoked a decrease in blood lactate and pyruvate but not in blood glucose concentrations. Urinary oxalate was not increased by the daily injection of 2 CP. Blood ketone body concentrations progressively increased after the third day of treatment. At the same time, plasma cholesterol slowly decreased. The 2 CP chronic administration did not change the plasma somatostatin, glucagon, and insulin levels. In the alloxan-diabetic dogs, treated with insulin alone, blood glucose, ketone body concentrations, and plasma somatostatin and glucagon levels were elevated. The adjunction of 2 CP with insulin injections resulted in a fall in blood lactate and pyruvate levels and a progressive decrease of blood glucose concentrations. Blood ketone bodies, which were already high at the start, were not affected when 2 CP was combined with insulin. The hypersomatostatinemia was not decreased, whereas the hyperglucagonemia was considerably reduced. So, I/G ratio, which was strongly decreased with insulin alone, progressively returned to normal values. As to urinary compounds, 2 CP induced a marked decrease in glucosuria and did not change the elevated urinary beta hydroxybutyrate levels. In conclusion, these findings show that the adjunction of sodium 2 chloropropionate to insulin in diabetic dogs results in a reduction of hyperglycemia and hyperglucagonemia.

Sodium 2-chloropropionate: its effects on experimental hyperlactatemia in the dog.

The effects of sodium 2-chloropropionate (2-CP), an activator of pyruvate dehydrogenase were studied on normal dogs. Two sets of experiments were performed: 1) 2-CP was administered to conscious dogs by gastric intubation at 1.16 mmol/kg b.wt. The drug induced a decrease in blood lactate and pyruvate levels but did not produce any significant change in blood glucose, blood beta-hydroxybutyrate or acetoacetate levels. 2) 2-CP given i.v. (1.16 mmol/kg b.wt. during 20 min) rapidly reduced the experimental hyperlactatemia induced by continuous infusion of epinephrine (1.5 microgram/kg . min) or fructose (0.5 g/kg . hr). Considering the metabolic side effects induced by dichloroacetate, another activator of pyruvate dehydrogenase, we suggest that use of 2-CP rather than dichloroacetate might be of interest, particularly in the treatment of hyperlactatemia or lactic acidosis.

[Kinetic aspects of the glipizide-induced hypoglycemia in the dog (author's transl)]. / Aspects cinétiques de l'hypoglycémie provoquée par le glipizide chez le chien.

The study of the kinetics of hypoglycemia induced by glipizide (second generation hypoglycemic sulfonamide) was carried out on the normal conscious dog. 1. In a first series of experiments glipizide was given intravenously at the dose of 0.1 mg .kg-1. The hypoglycemic effect of the drug occurred rapidly and reached a maximum at the 30th minute. This maximum effect did not much vary from one animal to another. The hypoglycemic action persisted at least 7 hours after the injection, and at the 24th hour blood glucose level returned practically to the initial values. 2. The kinetics of hypoglycemia after per os administration were studied when glipizide was given either in solid form preparation or in solution form. Glipizide given per os in powder form at the dose of 0.1 mg . kg-1 induced a kinetics of hypoglycemia which varied from one animal to another. The hypoglycemic effect which appeared within 1 to 4 hours after administration, reached its maximum within 2 to 6 hours; it ranged from -6 p. 100 to -52 p. 100. A tenfold higher dose (1 mg . kg-1) produced a hypoglycemia which occurred more rapidly, with less dispersion in the intensity of the response. When glipizide was given at the dose of 0.1 mg . kg-1 in solution form, it can be noted that in all cases hypoglycemia occurred earlier than after administration in powder form at the same dose, while the dispersion in the maximum effect is still considerable. These results lay stress once again on the importance of the form of administration on the kinetics of hypoglycemia and on its intensity.