Metabolic and Hormonal Alterations with Diacylglycerol and Low Glycemic Index Starch during Canine Weight Loss.

Obesity increases insulin resistance and disregulation of glucose homeostasis. This study investigated low glycemic index starch (LGIS)/diacylglycerol (DAG) diet on plasma insulin and circulating incretin hormones during canine weight loss. Obese Beagle dogs were fed one of four starch/oil combination diets (LGIS/DAG; LGIS/triacylglycerol (TAG); high glycemic index starch (HGIS)/DAG; and HGIS/TAG) for 9 weeks during the weight loss period. At weeks 1 and 8, fasting plasma insulin, glucose, nonesterified fatty acid (NEFA), glucose-dependent insulinotropic polypeptide (GIP), and glucagon-like peptide-1 (GLP-1) were determined. Weight loss did not affect fasting insulin, glucose, and NEFA, but fasting GIP increased and GLP-1 decreased. LGIS affected postprandial insulin at both times and glucose was similar to insulin, except 60 min postprandially with DAG at week 8. NEFA lowering was less with the LGIS diets initially but not thereafter. At 60 min postprandially on week 8, GIP was significantly elevated by DAG, while GLP-1 was increased only with the HD diet. LGIS suppressed insulin and glucose responses up to 180 min postprandially at both sample times. DAG increased incretin hormones as did the DAG/HGIS combination but only at week 8. This latter finding appeared to be related to the glucose response but not to insulin at 60 min.

Postprandial lipid-related metabolites are altered in dogs fed dietary diacylglycerol and low glycemic index starch during weight loss.

In this study, we investigated a combination of a low glycemic index starch (LGIS) and diacylglycerol (DAG) on lipid, lipoprotein (LP) metabolism, and weight management. Obese, intact female adult Beagle dogs were assigned to 1 of 4 starch/oil combination diets [LGIS/DAG (LD); LGIS/triacylglycerol (TAG); high glycemic index starch (HGIS)/DAG; and HGIS/TAG (HT)] and fed for 9 wk (n = 6/group) using an incomplete 4 × 4 Latin square design. Each dog was fed 1 of 2 opposite starch/oil combination diets (e.g. LD and HT). At wk 1 and 8, postprandial blood was collected for plasma triacylglycerol (TG), ß-hydroxybutyrate (BHB), total cholesterol (TC), and LP analyses. During the same week, dogs were overnight feed-deprived and post-heparin blood was collected for LP lipase and hepatic lipase activity determinations. At wk 1, 4, and 8, blood was drawn from overnight feed-deprived dogs for plasma TG, BHB, TC, LP, leptin, and adiponectin measurements. Feces were collected at wk 3 for digestibility calculations. The LGIS diets resulted in lower carbohydrate, protein, total tract dry matter digestibilities, and metabolizable energy compared with the HGIS diet groups (P < 0.05). Thus, the LGIS groups lost more body weight (P = 0.001), which was positively correlated with plasma leptin concentrations (r(2) = 0.427; P < 0.001). Moreover, the LGIS diet lowered TC concentrations in combination with DAG. The DAG diet groups decreased postprandial TG and increased BHB concentrations (P < 0.05). Starch/oil types did not alter lipase activities or adiponectin concentrations. In conclusion, the LGIS diet demonstrated potential as a weight management tool in dogs by decreasing postprandial TG and increasing BHB in combination with DAG.

Reduction of brain infarction induced by a transient brain ischemia in mdr1a knockout mice.

In order to evaluate the functional role of P-glycoprotein (P-gp) in cerebral ischemia, both multidrug resistance 1a knockout (KO) mice and wild-type mice were subjected to transient focal ischemia under a constant body and brain temperature about 37 degrees C. The results showed that the volume of brain infarction induced by middle cerebral artery occlusion in KO mice was significantly smaller than that seen in wild-type mice, although there were no significant differences in cerebral blood flow, physiological data and on anatomical analysis of cerebrovasculature between both groups. We suggest that multidrug resistance 1a P-gp plays a role for adjusting the expressions of endogenous neuronal cell modulating substances, such as cytokines, neuronal peptides, and others, in the brain, which is consistent with a previous paper (Bobrov et al. Neurosci Lett 24: 6-11, 2008).

Isoflurane inhibits protein kinase Cgamma and calcium/calmodulin dependent protein kinase ii-alpha translocation to synaptic membranes in ischemic mice brains.

Volatile anesthetics isoflurane possibly improves the ischemic brain injury. However, its molecular actions are still unclear. In ischemia, protein kinase C (PKC)gamma and calcium/calmodulin dependent protein kinase II (CaMKII)-alpha are persistently translocated from cytosol to cell membranes, and diminish these translocation suggested to be neuroprotective. We thus tested a hypothesis that isoflurane inhibits PKCgamma and CaMKII-alpha translocation after ischemic brain insults. C57Bl/6J male mice were made to inhale 1 or 2 MAC isoflurane, after which 3 or 5 min cerebral ischemia was induced by decapitation. The sampled cerebrum cortex was then homogenized and centrifuged into crude synaptosomal fractions (P2), cytosolic fractions (S3), and particulate fractions (P3). CaMKII-alpha and PKCgamma levels of these fractions were analyzed by immunoblotting. PKCgamma and CaMKII-alpha are translocated to synaptic membrane from cytosol by cerebral ischemia, although isoflurane significantly inhibited such translocation. These results may explain in part the cellular and molecular mechanisms of neuroprotective effects of isoflurane.

Ultracytochemical demonstration of glycoproteins in the canine knee synovium.

By various ultracytochemical methods, glycoconjugates of the synoviocytes, the intercellular matrix and the wall of the small capillaries were studied in the synovial intimal tissues of the canine knee joint. Glycoconjugates with vicinal diol groups could be visualized in certain elements of the Golgi complex, lysosomes, vacuoles, the majority of intracellular cytomembranes, the surface coat of the plasma membrane and glycogen particles in type A cells. In type B cells, less-developed Golgi complexes, and fewer lysosomes and vacuoles were present in the cytoplasm than in that of type A cells. In contrast, a large number of cytoplasmic glycogen particles and abundant vicinal diol-containing groups in the surface coat of the plasma membrane became especially obvious in the B cells. Abundant neutral and acidic glycoproteins were observed in fibrous components in the intercellular matrix. In the small capillaries, strongly positive staining intensities for neutral and acidic glycoconjugates were observed in the basement membrane and perivascular connective tissue, as well as in the surface coat of the luminal plasma membrane of the endothelial cells, although to a somewhat weaker degree. Sialic acid, particularly, was notable in the surface coat of the latter cells. In addition, glycoproteins in the type A cells were shown by lectin ultracytochemistry to contain a variety of saccharide residues such as alpha-D-mannose, alpha-D-glucose, alpha-L-fucose, N-acetyl-beta-D-glucosamine, and N-acetyl-neuraminic acid, which were also found in the plasma membrane of the B cells. The properties of the glycoconjugates found are discussed in relation to the basic functions assigned to the synovial membrane of the canine knee joint.