Dietary mannoheptulose does not alter glucose or lipid metabolism in adult Labrador Retrievers.

Mannoheptulose (MH), a glycolytic inhibitor, has been preliminarily investigated as a novel functional food ingredient for dogs. This study aimed to determine the effects of dietary MH, delivered as an extract of un-ripened avocados, on fatty acid and glucose kinetics in healthy adult Labrador Retriever dogs (n = 12 dogs). The study was a double-blindcrossover with each dog receiving both dietary treatments, control (CON) and MH (400 mg/kg of diet), in random order. Glucose and glycerol plasma turnover (Ra) and oxidation (Ox) were measured in fasting and in response to repeated meal feeding ("fed") with stable isotope tracers (U-13 C-glucose, 1,1,2,3,3-D5 -glycerol) and indirect calorimetry. Palmitate Ra and Ox were examined during repeated meal feeding only using an oral bolus of U-13 C-K2 -palmitate and indirect calorimetry. MH had no discernible effect on fasting glucose Ra (677, 722 SEM 36 µmol/min, CON, MH) or Ox (107, 109 µmol/min, CON, MH SEM 10 µmol/min) or fed glucose Ra (2913, 3626 SEM 644 µmol/min, CON, MH) or Ox (951, 936 SEM 174 µmol/min, CON, MH). Glycerol Ra, an index of the rate of lipolysis, was not different between dietary treatments (Fast 162, 113 SEM 35 µmol/min CON, MH; Fed 172, 135 SEM 21 µmol/min, CON, MH). Similarly, palmitate oxidation was not impacted by MH feeding (1966, 2276 SEM 79 µmol/min, CON, MH). Together, these findings do not support MH as a novel functional food ingredient at least at the dietary dose tested.

Dietary Mannoheptulose Does Not Significantly Alter Daily Energy Expenditure in Adult Labrador Retrievers.

Mannoheptulose (MH), a sugar found in avocados that inhibits glycolysis in vitro, has been preliminarily investigated as a novel food ingredient for dogs. This study aimed to determine the effects of dietary MH, delivered as an extract of un-ripened avocado, on energy expenditure (EE) in healthy adult Labrador Retriever dogs (total of 12 dogs, 26.99 ± 0.634 kg, 4.9 ± 0.2 y). The study was a double-blind, cross-over with each dog receiving both dietary treatments, control (CON) and MH (400 mg/kg of diet; 6 mg/kg BW), in random order. Resting and post-prandial (10 h) EE and respiratory quotient (RQ) were determined by indirect calorimetry (d 42). The following day, body composition was assessed using dual X-ray absorptiometry. Continuous activity monitoring was conducted using an Atical® accelerometer (d 43-47). A vastus lateralis muscle biopsy was obtained prior to the morning meal (d 49) and 4 h after consumption of their meal (d 56) to determine the protein content and phosphorylation of 5' adenosine monophosphate-activated protein kinase (AMPK). Diet did not affect body weight, resting EE or skeletal muscle AMPK phosphorylation. Dogs fed MH had significantly lower post-prandial RQ (p = 0.02) and ratio of fat to lean body mass (p = 0.02). Physical activity during light time periods (but not dark) was lower in dogs fed MH (p < 0.05) during weekends, but not on weekdays. These results suggest that MH affects energy balance of adult dogs, but that these effects are not dose dependent and not due to physical activity.

Brain glucosamine boosts protective glucoprivic feeding.

The risk of iatrogenic hypoglycemia is increased in diabetic patients who lose defensive glucoregulatory responses, including the important warning symptom of hunger. Protective hunger symptoms during hypoglycemia may be triggered by hypothalamic glucose-sensing neurons by monitoring changes downstream of glucose phosphorylation by the specialized glucose-sensing hexokinase, glucokinase (GK), during metabolism. Here we investigated the effects of intracerebroventricular (ICV) infusion of glucosamine (GSN), a GK inhibitor, on food intake at normoglycemia and protective feeding responses during glucoprivation and hypoglycemia in chronically catheterized rats. ICV infusion of either GSN or mannoheptulose, a structurally different GK inhibitor, dose-dependently stimulated feeding at normoglycemia. Consistent with an effect of GSN to inhibit competitively glucose metabolism, ICV coinfusion of d-glucose but not l-glucose abrogated the orexigenic effect of ICV GSN at normoglycemia. Importantly, ICV infusion of a low GSN dose (15 nmol/min) that was nonorexigenic at normoglycemia boosted feeding responses to glucoprivation in rats with impaired glucose counterregulation. ICV infusion of 15 nmol/min GSN also boosted feeding responses to threatened hypoglycemia in rats with defective glucose counterregulation. Altogether our findings suggest that GSN may be a potential therapeutic candidate for enhancing defensive hunger symptoms during hypoglycemia.

Assessment of islet beta-cell mass in isolated rat pancreases perfused with D-[(3)H]mannoheptulose.

D-mannoheptulose is apparently transported into cells mainly at the intervention of GLUT-2 and hence was recently proposed as a tool to label preferentially insulin-producing beta-cells in the pancreatic gland. The validity of such a proposal was investigated in the present study conducted in isolated perfused pancreatic glands from control and streptozotocin-induced diabetic rats. After a 30-min equilibration period, D-[(3)H]mannoheptulose (0.1 mM) and [U-(14)C]sucrose (0.5 mM) were infused for 15 min in the presence of 30 mM D-glucose. The pancreatic glands were then perfused for 10 min with a nonradioactive medium during and after administration of cytochalasin B (0.02 mM). Under these experimental conditions, the intracellular distribution space of D-[(3)H]mannoheptulose averaged 5.42 +/- 0.75 nl/mg in control animals, whereas it failed to be significantly different from zero in the streptozotocin rats. The present procedure may thus allow the assessment of the relative contribution of islet beta-cells to the total mass of the pancreatic gland.

Effect of combined treatment of anti-inflammatory drug and mannoheptulose on the production of tumour necrosis factor and endotoxin shock in mice.

The endotoxin shock induced in mice by injection of viable Listeria monocytogenes and challenged with endotoxin can be alleviated by combined administration of mannoheptulose with acetylsalicylate or sulindac. The ability of animals to secrete tumour necrosis factor into the blood was, however, not affected. The significance of these observations are discussed.

The response of chickens to D-mannoheptulose: feeding behavior and blood glucose.

Administration of mannoheptulose (MH) at a concentration of 200-300 mg./kg. body weight, administered intraperitoneally or intracardiacly resulted in a significant increase of plasma glucose concentration (24.3%) four hours after administration. Food consumption was effected by administration of 300 mg./kg. body weight. There was a significant reduction in the mannoheptulose treated animals compared to the saline controls during the second and third hours of testing. The results were similar to those reported for mammals although the increase in plasma glucose concentration was not as drmatic in birds as it is in mammals. Food consumption studies in rat indicate a suppression, however, it is not significant as it was in this study.