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  • 1
    Online Resource
    Online Resource
    Normal physical activity obliterates the deleterious effects of a high-caloric intake
    American Physiological Society ; 2014
    In:  Journal of Applied Physiology Vol. 116, No. 3 ( 2014-02-01), p. 231-239
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 116, No. 3 ( 2014-02-01), p. 231-239
    Abstract: A high-caloric intake combined with a sedentary lifestyle is an important player in the development of type 2 diabetes mellitus (T2DM). The present study was undertaken to examine if the level of physical activity has impact on the metabolic effects of a high-caloric (+2,000 kcal/day) intake. Therefore, healthy individuals on a high-caloric intake were randomized to either 10,000 or 1,500 steps/day for 14 days. Step number, total energy expenditure, dietary records, neuropsychological tests, maximal oxygen uptake (V̇o 2max ), whole body dual-energy X-ray absorptiometry (DXA) and abdominal magnetic resonance imaging (MRI) scans, continuous glucose monitoring (CGM), and oral glucose tolerance tests (OGTT) with stable isotopes were performed before and after the intervention. Both study groups gained the same amount of body weight. However, the inactive group accumulated significantly more visceral fat compared with the active group. Following the 2-wk period, the inactive group also experienced a poorer glycemic control, increased endogenous glucose production, decreased hepatic insulin extraction, increased baseline plasma levels of total cholesterol and LDL, and a decreased cognitive function with regard to capacity of attention. In conclusion, we find evidence to support that habitual physical activity may prevent pathophysiological symptoms associated with diet-induced obesity.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00155.2013
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2014
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    SSG: 31
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  • 2
    Online Resource
    Online Resource
    Effect of subcutaneous injections of PYY 1-36 and PYY 3-36 on appetite, ad libitum energy intake, and plasma free fatty acid concentration in obese males
    American Physiological Society ; 2007
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 293, No. 2 ( 2007-08), p. E604-E609
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 293, No. 2 ( 2007-08), p. E604-E609
    Abstract: Intraveneous (iv) PYY 3-36 infusions have been reported to reduce energy intake (EI) in humans, whereas few studies exist on effects of PYY 1-36 . The aim of the present study was to examine effects of subcutaneous (sc) injections of PYY 1-36 and PYY 3-36 on appetite, ad libitum EI, plasma concentrations of PYY and free fatty acids (FFA) in obese males. Twenty-four males (BMI 27–40 kg/m 2 ) were randomly assigned to two groups receiving sc injections of either PYY 1-36 or PYY 3-36 in a blinded, placebo-controlled, dose-escalating, cross-over study. Subjects were studied 5 days in succession, with escalating doses of PYY 1-36 [saline, 50, 100, 150, and 200 pmol PYY 1-36 /kg lean body mass (LBM)], or PYY 3-36 (saline, 25, 50, 75, and 100 pmol PYY 3-36 /kg LBM), respectively. PYY injections resulted in dose-dependent increases in plasma PYY levels but no effect on EI in either the PYY 1-36 or the PYY 3-36 group. However, increasing doses of PYY 3-36 , but not PYY 1-36 , resulted in increased ratings of satiety and decreased ratings of hunger, thirst, and prospective food consumption. Although not dose dependently, significant elevation of plasma FFA was seen after injection of PYY 3-36 , but not PYY 1-36 . Although sc administration of PYY was well tolerated, it remains to be determined whether high-dose PYY 3-36 is sufficient in reducing EI in long-term trials, and if so, whether the reduction in EI occurs without nausea. PYY 1-36 is unlikely to be important in regulating energy intake. The PYY 3-36 administrations caused a non-dose-dependent mobilization of FFA, likely through a direct effect.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00153.2007
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
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  • 3
    Online Resource
    Online Resource
    Glucose stimulates neurotensin secretion from the rat small intestine by mechanisms involving SGLT1 and GLUT2, leading to cell depolarization and calcium influx
    American Physiological Society ; 2015
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 308, No. 12 ( 2015-06-15), p. E1123-E1130
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 308, No. 12 ( 2015-06-15), p. E1123-E1130
    Abstract: Neurotensin (NT) is a neurohormone produced in the central nervous system and in the gut epithelium by the enteroendocrine N cell. NT may play a role in appetite regulation and may have potential in obesity treatment. Glucose ingestion stimulates NT secretion in healthy young humans, but the mechanisms involved are not well understood. Here, we show that rats express NT in the gut and that glucose gavage stimulates secretion similarly to oral glucose in humans. Therefore, we conducted experiments on isolated perfused rat small intestine with a view to characterize the cellular pathways of secretion. Luminal glucose (20% wt/vol) stimulated secretion but vascular glucose (5, 10, or 15 mmol/l) was without effect. The underlying mechanisms depend on membrane depolarization and calcium influx, since the voltage-gated calcium channel inhibitor nifedipine and the K ATP channel opener diazoxide, which causes hyperpolarization, eliminated the response. Luminal inhibition of the sodium-glucose cotransporter 1 (SGLT1) (by phloridzin) eliminated glucose-stimulated release as well as secretion stimulated by luminal methyl-α-d-glucopyranoside (20% wt/vol), a metabolically inactive SGLT1 substrate, suggesting that glucose stimulates secretion by initial uptake by this transporter. However, secretion was also sensitive to GLUT2 inhibition (by phloretin) and blockage of oxidative phosphorylation (2-4-dinitrophenol). Direct K ATP channel closure by sulfonylureas stimulated secretion. Therefore, glucose stimulates NT secretion by uptake through SGLT1 and GLUT2, both causing depolarization either as a consequence of sodium-coupled uptake (SGLT1) or by closure of K ATP channels (GLUT2 and SGLT1) secondary to the ATP-generating metabolism of glucose.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00012.2015
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2015
    detail.hit.zdb_id: 1477331-4
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  • 4
    Online Resource
    Online Resource
    Regulation of urea synthesis during the acute-phase response in rats
    American Physiological Society ; 2013
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 304, No. 7 ( 2013-04-01), p. G680-G686
    Details
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 304, No. 7 ( 2013-04-01), p. G680-G686
    Abstract: The acute-phase response is a catabolic event involving increased waste of amino-nitrogen (N) via hepatic urea synthesis, despite an increased need for amino-N incorporation into acute-phase proteins. This study aimed to clarify the regulation of N elimination via urea during different phases of the tumor necrosis factor-α (TNF-α)-induced acute-phase response in rats. We used four methods to study the regulation of urea synthesis: We examined urea cycle enzyme mRNA levels in liver tissue, the hepatocyte urea cycle enzyme proteins, the in vivo capacity of urea-N synthesis (CUNS), and known humoral regulators of CUNS at 1, 3, 24, and 72 h after TNF-α injection (25 μg/kg iv rrTNF-α) in rats. Serum acute-phase proteins and their liver mRNA levels were also measured. The urea cycle enzyme mRNA levels acutely decreased and then gradually normalized, whereas the urea cycle enzyme proteins remained essentially unchanged over time. The CUNS rose after 3 h and then normalized. The acute-phase response was fully activated at 24 h with markedly increased serum levels of the acute-phase proteins. TNF-α acutely upregulated the CUNS. Later, despite the fully established 24-h acute-phase response and the decreased activity of the urea cycle enzyme genes, there was no change in the urea cycle enzyme proteins or the CUNS. Thus in no phase after the initiation of the acute-phase response was in vivo urea synthesis orchestrated in combination with acute-phase protein synthesis so as to limit N waste.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    URL: Article
    DOI: 10.1152/ajpgi.00416.2012
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2013
    detail.hit.zdb_id: 1477329-6
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  • 5
    Online Resource
    Online Resource
    Rapid gut growth but persistent delay in digestive function in the postnatal period of preterm pigs
    American Physiological Society ; 2016
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 310, No. 8 ( 2016-04-15), p. G550-G560
    Details
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 310, No. 8 ( 2016-04-15), p. G550-G560
    Abstract: Preterm infants often tolerate full enteral nutrition a few weeks after birth but it is not known how this is related to gut maturation. Using pigs as models, we hypothesized that intestinal structure and digestive function are similar in preterm and term individuals at 3–4 wk after birth and that early enteral nutrition promotes maturation. Preterm or term cesarean-delivered pigs were fed total parenteral nutrition, or partial enteral nutrition [Enteral (Ent), 16–64 ml·kg −1 ·day −1 of bovine colostrum] for 5 days, followed by full enteral milk feeding until day 26. The intestine was collected for histological and biochemical analyses at days 0, 5, and 26 ( n = 8–12 in each of 10 treatment groups). Intestinal weight (relative to body weight) was reduced in preterm pigs at 0–5 days but ENT feeding stimulated the mucosal volume and peptidase activities. Relative to term pigs, mucosal volume remained reduced in preterm pigs until 26 days although plasma glucagon-like peptide 2 (GLP-2) and glucose-dependent insulin-trophic peptide (GIP) levels were increased. Preterm pigs also showed reduced hexose absorptive capacity and brush-border enzyme (sucrase, maltase) activities at 26 days, relative to term pigs. Intestinal structure shows a remarkable growth adaptation in the first week after preterm birth, especially with enteral nutrition, whereas some digestive functions remain immature until at least 3–4 wk. It is important to identify feeding regimens that stimulate intestinal maturation in the postnatal period of preterm infants because some intestinal functions may show long-term developmental delay.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    URL: Article
    DOI: 10.1152/ajpgi.00221.2015
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2016
    detail.hit.zdb_id: 1477329-6
    SSG: 12
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