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  • 1
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    Hepatic glucose disposition during concomitant portal glucose and amino acid infusions in the dog
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 274, No. 5 ( 1998-05-01), p. E893-E902
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 274, No. 5 ( 1998-05-01), p. E893-E902
    Abstract: The effect of concomitant intraportal infusion of glucose and gluconeogenic amino acids (AA) on net hepatic glucose uptake (NHGU) and glycogen synthesis was examined in 42-h-fasted dogs. After a basal period, there was a 240-min experimental period during which somatostatin was infused continuously into a peripheral vein and insulin and glucagon (at 3-fold basal and basal rates, respectively) and glucose (18.3 μmol ⋅ kg −1 ⋅ min −1 ) were infused intraportally. One group (PoAA, n = 7) received an AA mixture intraportally at 7.6 μmol ⋅ kg −1 ⋅ min −1 , whereas the other group (NoAA, n = 6) did not receive AA. Arterial blood glucose concentrations and hepatic glucose loads were the same in the two groups. NHGU averaged 4.8 ± 2.0 (PoAA) and 9.4 ± 2.0 (NoAA) μmol ⋅ kg −1 ⋅ min −1 ( P 〈 0.05), and tracer-determined hepatic glucose uptake was 4.6 ± 1.6 (PoAA) and 10.0 ± 1.7 (NoAA) μmol ⋅ kg −1 ⋅ min −1 ( P 〈 0.05). AA data for PoAA and NoAA, respectively, were as follows: arterial blood concentrations, 1,578 ± 133 vs. 1,147 ± 86 μM ( P 〈 0.01); hepatic loads, 56 ± 3 vs. 32 ± 4 μmol ⋅ kg −1 ⋅ min −1 ( P 〈 0.01); and net hepatic uptakes, 14.1 ± 1.4 vs. 5.6 ± 0.4 μmol ⋅ kg −1 ⋅ min −1 ( P 〈 0.01). The rate of net hepatic glycogen synthesis was 7.5 ± 1.9 (PoAA) vs. 10.7 ± 2.3 (NoAA) μmol ⋅ kg −1 ⋅ min −1 ( P = 0.1). In a net sense, intraportal gluconeogenic amino acid delivery directed glucose carbon away from the liver. Despite this, net hepatic carbon uptake was equivalent in the presence and absence of amino acid infusion.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.1998.274.5.E893
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
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  • 2
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    Hyperglycemia compensates for diet-induced insulin resistance in liver and skeletal muscle of rats
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 281, No. 5 ( 2001-11-01), p. R1380-R1389
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 281, No. 5 ( 2001-11-01), p. R1380-R1389
    Abstract: High-fat and high-sucrose diets increase the contribution of gluconeogenesis to glucose appearance (glc R a ) under basal conditions. They also reduce insulin suppression of glc R a and insulin-stimulated muscle glycogen synthesis under euglycemic, hyperinsulinemic conditions. The purpose of the present study was to determine whether these impairments influence liver and muscle glycogen synthesis under hyperglycemic, hyperinsulinemic conditions. Male rats were fed a high-sucrose, high-fat, or low-fat, starch control diet for either 1 ( n = 5–7/group) or 5 wk ( n = 5–6/group). Studies involved two 90-min periods. During the first, a basal period (BP), [6- 3 H]glucose was infused. In the second, a hyperglycemic period (HP), [6- 3 H]glucose, [6- 14 C]glucose, and unlabeled glucose were infused. Plasma glucose (BP: 111.2 ± 1.5 mg/dl; HP: 172.3 ± 1.5 mg/dl), insulin (BP: 2.5 ± 0.2 ng/ml; HP: 4.9 ± 0.3 ng/ml), and glucagon (BP: 81.8 ± 1.6 ng/l; HP: 74.0 ± 1.3 ng/l) concentrations were not significantly different among diet groups or with respect to time on diet. There were no significant differences among groups in the glucose infusion rate (mg · kg −1 · min −1 ) necessary to maintain arterial glucose concentrations at ∼170 mg/dl (pooled average: 6.4 ± 0.8 at 1 wk; 6.4 ± 0.7 at 5 wk), percent suppression of glc R a (44.4 ± 7.8% at 1 wk; 63.2 ± 4.3% at 5 wk), tracer-estimated net liver glycogen synthesis (7.8 ± 1.3 μg · g liver −1 · min −1 at 1 wk; 10.5 ± 2.2 μg · g liver −1 · min −1 at 5 wk), indirect pathway glycogen synthesis (3.7 ± 0.9 μg · g liver −1 · min −1 at 1 wk; 3.4 ± 0.9 μg · g liver −1 · min −1 at 5 wk), or tracer-estimated net muscle glycogenesis (1.0 ± 0.3 μg · g muscle −1 · min −1 at 1 wk; 1.6 ± 0.3 μg · g muscle −1 · min −1 at 5 wk). These data suggest that hyperglycemia compensates for diet-induced insulin resistance in both liver and skeletal muscle.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.2001.281.5.R1380
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477297-8
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  • 3
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    A high-sucrose diet increases gluconeogenic capacity in isolated periportal and perivenous rat hepatocytes
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 280, No. 5 ( 2001-05-01), p. E695-E702
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 280, No. 5 ( 2001-05-01), p. E695-E702
    Abstract: A high-sucrose (SU) diet increases gluconeogenesis (GNG) in the liver. The present study was conducted to determine the contribution of periportal (PP) and perivenous (PV) cell populations to this SU-induced increase in GNG. Male Sprague-Dawley rats were fed an SU (68% sucrose) or starch (ST, 68% starch) diet for 1 wk, and hepatocytes were isolated from the PP or PV region of the liver acinus. Hepatocytes were incubated for 1 h in the presence of various gluconeogenic substrates, and glucose release into the medium was used to estimate GNG. When incubated in the presence of 5 mM lactate, which enters GNG at the level of pyruvate, glucose release (nmol · h −1 · mg −1 ) was significantly increased by the SU diet in both PP (84.8 ± 3.4 vs. 70.4 ± 2.6) and PV (64.3 ± 2.5 vs. 38.2 ± 2.1) cells. Addition of palmitate (0.5 mM) increased glucose release from lactate in PP cells by 11.6 ± 0.5 and 20.6 ± 1.5% and in PV cells by 11.0 ± 4.4 and 51.1 ± 9.1% in SU and ST, respectively. When cells were incubated with 5 mM dihydroxyacetone (DHA), which enters GNG at the triosephosphate level, glucose release was significantly increased by the SU diet in both cell types. In contrast, glucose release from fructose (0.5 mM) was significantly increased by the SU diet in PV cells only. These changes in glucose release were accompanied by significant increases in the maximal specific activities of glucose-6-phosphatase (G-6-Pase) and phospho enolpyruvate carboxykinase (PEPCK) in both PP and PV cells. These data suggest that the SU diet influences GNG in both PP and PV cell populations. It appears that SU feeding produces changes in GNG via alterations in at least two critical enzymes, G-6-Pase and PEPCK.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.2001.280.5.E695
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
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  • 4
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    Docosahexaenoic Acid Supplementation Does Not Improve Western Diet-Induced Cardiomyopathy in Rats
    Public Library of Science (PLoS) ; 2012
    In:  PLoS ONE Vol. 7, No. 12 ( 2012-12-26), p. e51994-
    Details
    In: PLoS ONE, Public Library of Science (PLoS), Vol. 7, No. 12 ( 2012-12-26), p. e51994-
    Type of Medium: Online Resource
    ISSN: 1932-6203
    URL: Article
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    DOI: 10.1371/journal.pone.0051994
    DOI: 10.1371/journal.pone.0051994.g001
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    DOI: 10.1371/journal.pone.0051994.t001
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    DOI: 10.1371/journal.pone.0051994.s001
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    DOI: 10.1371/journal.pone.0051994.s007
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2012
    detail.hit.zdb_id: 2267670-3
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  • 5
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    Diets enriched in sucrose or fat increase gluconeogenesis and G-6-Pase but not basal glucose production in rats
    American Physiological Society ; 2002
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 283, No. 3 ( 2002-09-01), p. E545-E555
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 283, No. 3 ( 2002-09-01), p. E545-E555
    Abstract: High-fat (HFD) and high-sucrose diets (HSD) reduce insulin suppression of glucose production in vivo, increase the capacity for gluconeogenesis in vitro, and increase glucose-6-phosphatase (G-6-Pase) activity in whole cell homogenates. The present study examined the effects of HSD and HFD on in vivo gluconeogenesis, the catalytic and glucose-6-phosphate translocase subunits of G-6-Pase, glucokinase (GK) translocation, and glucose cycling. Rats were fed a high-starch control diet (STD; 68% cornstarch), HSD (68% sucrose), or HFD (45% fat) for 7–13 days. The ratio of 3 H in C6:C2 of glucose after 3 H 2 O injection into 6- to 8-h-fasted rats was significantly increased in HSD (0.68 ± 0.07) and HFD (0.71 ± 0.08) vs. STD (0.40 ± 0.10). G-6-Pase activity was significantly higher in HSD and HFD vs. STD in both intact and disrupted liver microsomes. HSD and HFD significantly increased the amount of the p36 catalytic subunit protein, whereas the p46 glucose-6-phosphate translocase protein was increased in HSD only. Despite increased nonglycerol gluconeogenesis and increased G-6-Pase, basal glucose and insulin levels as well as glucose production were not significantly different among groups. Hepatocyte cell suspensions were used to ascertain whether diet-induced adaptations in glucose phosphorylation and GK might serve to compensate for upregulation of G-6-Pase. Tracer-estimated glucose phosphorylation and glucose cycling (glucose ↔ glucose 6-phosphate) were significantly higher in cells isolated from HSD only. After incubation with either 5 or 20 mM glucose and no insulin, GK activity (nmol · mg protein −1 · min −1 ) in digitonin-treated eluates (translocated GK) was significantly higher in HSD (32 ± 4 and 146 ± 6) vs. HFD (4 ± 1 and 83 ± 10) and STD (9 ± 2 and 87 ± 9). Thus short-term, chronic exposure to HSD and HFD increase in vivo gluconeogenesis and the G-6-Pase catalytic subunit. Exposure to HSD diet also leads to adaptations in glucose phosphorylation and GK translocation.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00120.2002
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2002
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  • 6
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    Elevated basal PI 3-kinase activity and reduced insulin signaling in sucrose-induced hepatic insulin resistance
    American Physiological Society ; 2002
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 282, No. 1 ( 2002-01-01), p. E170-E176
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 282, No. 1 ( 2002-01-01), p. E170-E176
    Abstract: Sucrose feeding reduces the ability of insulin to suppress glucose production and hepatic gluconeogenesis. The present study examined the effect of a high-sucrose diet on early insulin-signaling steps in the liver. Rats were provided a high-starch (STD, control diet) or high-sucrose diet (HSD) for 3 wk. On the day of study, overnight-fasted rats were anesthetized and injected with either saline ( n = 5/diet group) or insulin (2 mU/kg, n = 5/diet group) via the portal vein. Portal venous blood and liver tissue were harvested 2 min after injections. Portal vein plasma glucose levels were not significantly different among groups, pooled average 147 ± 12 mg/dl. Western blot analysis revealed no significant differences in the amount of insulin receptor (IR), insulin receptor substrates-1 and -2 (IRS-1, IRS-2), and the p85 subunit of phosphatidylinositol (PI) 3-kinase. In contrast, the amount of the p110β subunit of PI 3-kinase was increased ∼2-fold in HSD vs. STD ( P 〈 0.05). After saline injection, tyrosine phosphorylation (pY) of IR, IRS-1, and IRS-2 was not significantly different between groups. However, PI 3-kinase activity associated with phosphorylated proteins was increased ∼40% in HSD vs. STD ( P 〈 0.05). After insulin injection, pY of the IR was not different between groups, whereas pY of IRS-1 and IRS-2 was reduced ( P 〈 0.05) in HSD vs. STD. In addition, association of IRS-1 and IRS-2 with p85 was significantly reduced in HSD vs. STD. These data demonstrate that an HSD impairs insulin-stimulated early postreceptor signaling (pY of IRS proteins, IRS interaction with p85). Furthermore, the increased amount of p110β and increased basal PI 3-kinase activity suggest a diet-induced compensatory response.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.2002.282.1.E170
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2002
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  • 7
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    Increased pyruvate flux capacities account for diet-induced increases in gluconeogenesis in vitro
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 281, No. 2 ( 2001-08-01), p. R427-R433
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 281, No. 2 ( 2001-08-01), p. R427-R433
    Abstract: High-fat (HF) and high-sucrose (SU) diets increase gluconeogenesis. The present study was designed to determine the contributions of pyruvate dehydrogenase, pyruvate carboxylase, phospho enolpyruvate carboxykinase (PEPCK), and pyruvate kinase fluxes to this accelerated gluconeogenesis (GNEO) in the absence and presence of fatty acids. Male Sprague-Dawley rats were fed an HF, SU, or starch (ST) diet for 1 wk, and hepatocytes or mitochondria were isolated. In the absence of palmitate, the tracer estimated rates of GNEO (nmol · min −1 · mg −1 ) were elevated in hepatocytes isolated from SU (32.3 ± 1.8) and HF (35.4 ± 1.8) vs. ST (22.8 ± 1.5). Pyruvate carboxylase and PEPCK flux rates (nmol · min −1 · mg −1 ) were increased in the SU (47.5 ± 2.2 and 34.8 ± 1.5) and HF (49.4 ± 1.8 and 38.2 ± 1.8) groups compared with the ST group (32.8 ± 3.2 and 44.3 ± 2.0). Palmitate (250–1,000 μM) stimulation of these fluxes was not significantly different among groups. Bromopalmitate, an inhibitor of fat oxidation, abolished differences in GNEO, pyruvate carboxylase, and PEPCK fluxes in HF and SU vs. ST. In isolated mitochondria, pyruvate carboxylation and palmitoyl carnitine oxidation were not significantly different among groups. The results of this study suggest that the increased gluconeogenic flux observed with HF and SU diets is associated with an increased pyruvate flux through pyruvate carboxylase and PEPCK. Moreover, the ability of bromopalmitate to normalize gluconeogenic fluxes suggests that endogenous fatty acids contribute to diet-induced increases in GNEO.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.2001.281.2.R427
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
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  • 8
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    Sucrose diets increase glucose-6-phosphatase and glucose release and decrease glucokinase in hepatocytes
    American Physiological Society ; 2001
    In:  Journal of Applied Physiology Vol. 91, No. 5 ( 2001-11-01), p. 2041-2046
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 91, No. 5 ( 2001-11-01), p. 2041-2046
    Abstract: A high-sucrose diet (SU) decreases insulin action in the liver (Pagliassotti MJ, Shahrokhi KA, and Moscarello M. Am J Physiol Regulatory Integrative Comp Physiol 266: R1637–R1644, 1994). The present study was conducted to characterize the effect of SU on glucagon action in isolated periportal (PP) and perivenous (PV) hepatocytes by measuring glucagon-stimulated glycogenolysis and glucose release. Male rats were fed a SU (68% sucrose) or starch diet (ST, 68% starch) for 1 wk, and hepatocytes were isolated from PP or PV regions ( n = 4/diet/cell population). Hepatocytes were incubated for 1 h in the presence of varying concentrations of glucagon (0–100 nM). In PP and PV cells, glucagon stimulation of glucose release and glycogenolysis (sum of glucose release and lactate accumulation) was not significantly different between SU and ST cells. However, in the SU PP cells, glucose release was increased compared with ST PP cells, both in the absence of glucagon (76.1 ± 4 vs. 54.8 ± 3 nmol · h −1 · mg cell wet wt −1 ) and at all glucagon concentrations. In SU-fed PV cells, glucose release was increased compared with ST PV cells in the absence of glucagon (79.3 ± 5 vs. 56.4 ± 5 nmol · h −1 · mg cell wet wt −1 ) and at low glucagon concentrations. Maximal glucose-6-phosphatase activity (in nmol · min −1 · mg protein −1 ) was elevated in SU compared with ST cells (61.4 ± 3 vs. 37.5 ± 4 in PP and 37.5 ± 4 vs. 29.5 ± 3 in PV cells). In contrast, maximal glucokinase activity (in nmol · min −1 · mg protein −1 ) was elevated in ST compared with SU cells (15.9 ± 2 vs. 12.1 ± 1 in PP and 19.4 ± 2 vs. 14.2 ± 1 in PV cells). These data demonstrate that SU increases the capacity for glucose release in both PP and PV hepatocytes, in part because of reciprocal changes in glucose-6-phosphatase and glucokinase.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.2001.91.5.2041
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1404365-8
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  • 9
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    Hepatic adaptations to sucrose and fructose
    Elsevier BV ; 2005
    In:  Metabolism Vol. 54, No. 9 ( 2005-9), p. 1189-1201
    Details
    In: Metabolism, Elsevier BV, Vol. 54, No. 9 ( 2005-9), p. 1189-1201
    Type of Medium: Online Resource
    ISSN: 0026-0495
    URL: Article
    DOI: 10.1016/j.metabol.2005.04.004
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2005
    detail.hit.zdb_id: 2049062-8
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  • 10
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    An Acute Increase in Fructose Concentration Increases Hepatic Glucose-6-Phosphatase mRNA via Mechanisms That Are Independent of Glycogen Synthase Kinase-3 in Rats
    Elsevier BV ; 2004
    In:  The Journal of Nutrition Vol. 134, No. 3 ( 2004-03), p. 545-551
    Details
    In: The Journal of Nutrition, Elsevier BV, Vol. 134, No. 3 ( 2004-03), p. 545-551
    Type of Medium: Online Resource
    ISSN: 0022-3166
    URL: Article
    DOI: 10.1093/jn/134.3.545
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2004
    detail.hit.zdb_id: 1469429-3
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