Home About us Contact
|
Home About us Contact | ||
|
|
||
Physiologic Adaptation (physiologic + adaptation)
Selected AbstractsRegulation of protein phosphatase 1, activity in hypoxia through increased interaction with NIPP1: Implications for cellular metabolismJOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2006Kathrina M. Comerford Eukaryotic cells sense decreased oxygen levels and respond by altering their metabolic strategy to sustain non-respiratory ATP production through glycolysis, and thus promote cell survival in a hypoxic environment. Protein phosphatase 1 (PP1) has been recently implicated in the governance of the rational use of energy when metabolic substrates are abundant and contributes to cellular recovery following metabolic stress. Under conditions of hypoxia, the expression of the gamma isoform of PP1 (PP1,), is diminished, an event we have hypothesized to be involved in the adaptive cellular response to hypoxia. Decreased PP1, activity in hypoxia has a profound impact on the activity of the cAMP response element binding protein (CREB), a major transcriptional regulator of metabolic genes and processes. Here, we demonstrate a further mechanism leading to inhibition of PP1 activity in hypoxia which occurs at least in part through increased association with the nuclear inhibitor of PP1 (NIPP1), an event dependent upon decreased basal cAMP/PKA-dependent signaling. Using a dominant negative NIPP1 construct, we provide evidence that NIPP1 plays a major role in the regulation of both CREB protein expression and CREB-dependent transcription in hypoxia. Furthermore, we demonstrate functional sequellae of such events including altered gene expression and recovery of cellular ATP levels. In summary, we demonstrate that interaction with NIPP1 mediates decreased PP1, activity in hypoxia, an event which may constitute an inherent part of the cellular oxygen-sensing machinery and may play a role in physiologic adaptation to hypoxia. J. Cell. Physiol. 209: 211,218, 2006. © 2006 Wiley-Liss, Inc. [source] Adrenergic regulation of cardiac myocyte apoptosisJOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2001Krishna Singh The direct effects of catecholamines on cardiac myocytes may contribute to both normal physiologic adaptation and pathologic remodeling, and may be associated with cellular hypertrophy, apoptosis, and alterations in contractile function. Norepinephrine (NE) signals via ,- and ,-adrenergic receptors (AR) that are coupled to G-proteins. Pharmacologic studies of cardiac myocytes in vitro demonstrate that stimulation of ,1 -AR induces apoptosis which is cAMP-dependent and involves the voltage-dependent calcium influx channel. In contrast, stimulation of ,2 -AR exerts an anti-apoptotic effect which appears to be mediated by a pertussis toxin-sensitive G protein. Stimulation of ,1 -AR causes myocyte hypertrophy and may exert an anti-apoptotic action. In transgenic mice, myocardial overexpression of either ,1 -AR or G,s is associated with myocyte apoptosis and the development of dilated cardiomyopathy. Myocardial overexpression of ,2 -AR at low levels results in improved cardiac function, whereas expression at high levels leads to dilated cardiomyopathy. Overexpression of wildtype ,1B -AR does not result in apoptosis, whereas overexpression of G,q results in myocyte hypertrophy and/or apoptosis depending on the level of expression. Differential activation of the members of the mitogen-activated protein kinase (MAPK) superfamily and production of reactive oxygen species appear to play a key role in mediating the actions of adrenergic pathways on myocyte apoptosis and hypertrophy. This review summarizes current knowledge about the molecular and cellular mechanisms involved in the regulation of cardiac myocyte apoptosis via stimulation of adrenergic receptors and their coupled effector pathways. © 2001 Wiley-Liss, Inc. [source] Health-Related Hardiness and Chronic Illness: A Synthesis of Current ResearchNURSING FORUM, Issue 3 2003Mirella Vasquez Brooks APRN, PhD(C) TOPIC A critical analysis of the relationship between health-related hardiness and chronic illnesses based on a review of the literature. PURPOSE To synthesize the current literature in order to provide an understanding of the state of knowledge and the implications for nursing regarding health-related hardiness and chronic illness. SOURCES Three computerized databases, which yielded 125 articles published from 1966 to 2002. CONCLUSIONS The presence of the health-related hardiness characteristic was significantly related to psychological, psychosocial, and physiologic adaptation. Higher levels of hardiness had positive outcomes in patients with chronic illness. The implications are that the current knowledge base regarding health-related hardiness and chronic illness could be used to assist patients who have to manage not only one but also multiple chronic illnesses. [source] Insulin resistance of puberty in African-American children: lack of a compensatory increase in insulin secretionPEDIATRIC DIABETES, Issue 1 2002Rola J. Saad Abtract: Type 2 diabetes has been increasing in children, mostly affecting minority populations at around the age of puberty. Despite a multitude of studies demonstrating pubertal insulin resistance/hyperinsulinemia in white children, data are almost non-existent in African-American children. The aim of the present study was to investigate the impact of puberty on glucose metabolism, insulin sensitivity and secretion in African-American children. Twenty prepubertal and 16 pubertal African-American subjects participated. All underwent a 3-h hyperinsulinemic (40 mU/m2/min) euglycemic clamp to determine insulin-stimulated glucose disposal, and a 2-h hyperglycemic (12.5 mmol/L) clamp to assess first- and second-phase insulin secretion. Body composition was assessed by dual energy X-ray absorptiometry (DEXA) and visceral and subcutaneous abdominal adiposity with computed tomography (CT) scan at L4,L5. Total glucose disposal, glucose oxidation and non-oxidative glucose disposal were significantly lower in the pubertal group compared with the prepubertal one (53.8 ± 3.9 vs. 72.2 ± 5.0 µmol/kg/min, p = 0.009; 23.3 ± 1.1 vs. 31.6 ± 1.7 µmol/kg/min, p = 0.001; and 30.0 ± 3.3 vs. 40.5 ± 3.9 µmol/kg/min, p = 0.049, respectively). Insulin sensitivity was ,30% lower in the adolescents compared with the prepubertal children. However, first- and second-phase insulin secretions were not different between the two groups (971.4 ± 180.6 vs. 1044.0 ± 191.4 pmol/L and 999.6 ± 159.6 vs. 955.8 ± 142.2 pmol/L, respectively). In conclusion, despite ,30% lower insulin sensitivity in African-American adolescents compared with prepubertal children, insulin secretion is not higher. This is in contrast to published findings in white children in whom insulin secretion is higher during puberty. These racial differences in physiologic adaptation to puberty could play a role in the higher prevalence of type 2 diabetes in African-American children at the time of puberty. [source] | ||||||||||