GLORIA

GEOMAR Library Ocean Research Information Access

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 293, No. 5 ( 2007-11), p. E1451-E1458
    Abstract: Individuals born with a low birth weight (LBW) have an increased prevalence of type 2 diabetes, but the mechanisms responsible for this association are unknown. Given the important role of insulin resistance in the pathogenesis of type 2 diabetes, we examined insulin sensitivity in a rat model of LBW due to intrauterine fetal stress. During the last 7 days of gestation, rat dams were treated with dexamethasone and insulin sensitivity was assessed in the LBW offspring by a hyperinsulinemic euglycemic clamp. The LBW group had liver-specific insulin resistance associated with increased levels of PEPCK expression. These changes were associated with pituitary hyperplasia of the ACTH-secreting cells, increased morning plasma ACTH concentrations, elevated corticosterone secretion during restraint stress, and an ∼70% increase in 24-h urine corticosterone excretion. These data support the hypothesis that prenatal stress can result in chronic hyperactivity of the hypothalamic-pituitary-adrenal axis, resulting in increased plasma corticosterone concentrations, upregulation of hepatic gluconeogenesis, and hepatic insulin resistance.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
    detail.hit.zdb_id: 1477331-4
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 2010
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 298, No. 5 ( 2010-05), p. G571-G581
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 298, No. 5 ( 2010-05), p. G571-G581
    Abstract: Gastroesophageal reflux disease (GERD) is one of the most common problems in clinical practice today. It is widely believed that functional and structural abnormalities of the gastroesophageal junction as well as an abnormal exposure to gastroduodenal contents are the main contributors to its pathogenesis. Novel findings of the inflammatory process in GERD suggest a far more complex process involving multifaceted inflammatory mechanisms. This review summarizes knowledge about the expression of inflammatory mediators in GERD and their potential cellular sources and provides an integrated concept of disease pathogenesis. In addition we evaluate the contribution of inflammatory mediators to well-known complications of GERD, namely motility abnormalities, fibrosis, and carcinogenesis. Novel findings regarding the pathophysiology of esophageal inflammation should enhance our understanding of GERD and its complications and provide new treatment insights.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1477329-6
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 274, No. 1 ( 1998-01-01), p. E130-E138
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 274, No. 1 ( 1998-01-01), p. E130-E138
    Abstract: To examine the effects of a physiological increase in plasma epinephrine concentration (∼800 pg/ml) on muscle glycogenolysis and insulin-stimulated glycogenesis, we infused epinephrine [1.2 μg ⋅ (m 2 body surface) −1 ⋅ min −1 ] for 2 h and monitored muscle glycogen and glucose 6-phosphate (G-6- P) concentrations with 13 C/ 31 P nuclear magnetic resonance (NMR) spectroscopy. Epinephrine caused an increase in plasma glucose (Δ ∼50 mg/dl), lactate (Δ ∼1.4 mM), free fatty acids (Δ ∼1,200 μM at peak), and whole body glucose oxidation (Δ ∼0.85 mg ⋅ kg −1 ⋅ min −1 ) compared with levels in a group of control subjects ( n = 4) in the presence of slight hyperinsulinemia (∼13 μU/ml, n = 8) or basal insulin (∼7 μU/ml, n = 7). However, epinephrine did not induce any detectable changes in glycogen or G-6- P concentrations, whereas muscle inorganic phosphate (P i ) decreased by 35%. Epinephrine infusion during a euglycemic-hyperinsulinemic clamp ( n = 8) caused a 45% decrease in the glucose infusion rate that could be mostly attributed to a 73% decrease in muscle glycogen synthesis rate. After an initial increase to ∼160% of basal values, G-6- Plevels decreased by ∼30% with initiation of the epinephrine infusion. We conclude that a physiological increase in plasma epinephrine concentration 1) has a negligible effect on muscle glycogenolysis at rest, 2) decreases muscle P i , which may maintain phosphorylase activity at a low level, and 3) causes a major impairment in insulin-stimulated muscle glycogen synthesis, possibly due to inhibition of glucose transport-phosphorylation activity.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1477331-4
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...