Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Nutrients metabolized

There is weak expression of PPARy in muscle, liver and other tissues, enabling TZDs to support the effects of insulin in these tissues, notably increased glucose uptake in muscle and reduced glucose production in liver. TZDs may also affect nutrient metabolism by skeletal muscle through a direct mitochondrial action that is independent of PPARy. [Pg.120]

Biological actions Adipocyte differentiation fatty acid uptake lipogenesis glucose uptake other effects on nutrient metabolism which lower hepatic glucose production... [Pg.121]

AHLs as Nutrients Metabolic and Chemical Conversions of AHLs.304... [Pg.291]

Nicotinate and nicotinamide, together referred to as niacin, are required for biosynthesis of the coenzymes nicotinamide adenine dinucleotide (NAD"") and nicotinamide adenine dinucleotide phosphate (NADP" ). These both serve in energy and nutrient metabolism as carriers of hydride ions (see pp. 32, 104). The animal organism is able to convert tryptophan into nicotinate, but only with a poor yield. Vitamin deficiency therefore only occurs when nicotinate, nicotinamide, and tryptophan are all simultaneously are lacking in the diet. It manifests in the form of skin damage (pellagra), digestive disturbances, and depression. [Pg.366]

Yang R, Castriota G, Chen Z et al (2011) RNAi-mediated germlme knockdown of FABP4 increases body weight but does not improve the deranged nutrient metabolism of diet-induced obese mice. Int J Obes 35 217-225... [Pg.323]

Thyroid hormones govern or regulate our metabolic-rate or metabolism. Metabolic rate is the speed or rate at which all chemical and physical processes occur. This is true of every living cell in our bodies. This means that the rate of nutrient metabolism, absorption, and utilization is vastly dependent upon thyroid hormones. In... [Pg.106]

Thyroid hormones can have a re-partitioning effect upon body composition or muscle-to-fat ratio. As example were the many athletes whose weight was 250 LBS but only 10% bodyfat when total daily circulating thyroid hormone levels were elevated 10-50%. This would be due to thyroid hormone activity inducing improved nutrient metabolization and cellular efficiency combined with other hormone synergy. Of course, this is what "Absolute Anabolic Phases" were all about. But those who read about" Frank N. Steroid" already know about this effect and how it was created. [Pg.107]

The house mouse, mus musculus, is characterized by its ability to live in close association with people. In fact, most have been dependant on human shelter and activity and have migrated along with human population for over 10,000 years. They are referred to as commensal animals because they share related food supplies. Mice like humans are omnivorous and overall are considered a good model to study the regulation of dietary intake and nutrient metabolism in humans. In addition, a wealth of information resources and experimental approaches for mouse genetics are available for the study of biological processes involved in human diseases (1). [Pg.136]

Feeding nutrients during the culture allows an increase of the total amount of nutrients metabolized by the cells, which results in higher final concentrations of cells and product. Effects of high initial nutrient concentrations can be eliminated, since the nutrients are not added all at once at the beginning of the process. [Pg.238]

Cook, M. E., Miller, C. C., Park, Y., and Pariza, M. W. 1993. Immune modulation by altered nutrient metabolism nutritional control of immune-induced growth depression. Poultry Sci., 72,1301-1305. [Pg.387]

Figure 4 The contribution of impaired metabolism to cardiovascular risk. A dysregulation in nutrient metabolism contributes to cardiovascular risk by the following mechanisms 1) impaired p-cell function, tissue damage, and insulin resistance 2) an atherogenic lipid profile that is characterized by high TG, low HDL, and abnormal lipoproteins 3) hypertension and vascular dysfunction and 4) alterations in cytokines and adipokines that lead to a proinflammatory and procoagulant state. Figure 4 The contribution of impaired metabolism to cardiovascular risk. A dysregulation in nutrient metabolism contributes to cardiovascular risk by the following mechanisms 1) impaired p-cell function, tissue damage, and insulin resistance 2) an atherogenic lipid profile that is characterized by high TG, low HDL, and abnormal lipoproteins 3) hypertension and vascular dysfunction and 4) alterations in cytokines and adipokines that lead to a proinflammatory and procoagulant state.
E)rug5 that influence nutrient metabolism are discussed in various sections. These drugs include lovastatin, pravastatin, omeprazole, dilantin, methotrexate, allopurinol, warfarin, furosemide, thiouracil, and diphosphonatc. Alcohol is also discussed in this context because, depending on its intake, it functions as a food, drug, or toxin. [Pg.1022]

Changes in body weight, nutrient metabolism, adrenal cortical activity, and blood chemistry were observed in guinea pigs following inhalation of 1.5% for up to 91 days. Rats on chronic exposure have had reversible tissue changes in the central nervous system, lungs, liver, kidneys, and muscle tissue of the heart. [Pg.419]

Initiators of insulin secretion switch on the secretory machinery. Thereafter modulators derived from nutrient metabolism, hormones/peptides and neurotransmitters determine how fast or slow the machine will run. [Pg.79]

Fig. 20. Hypothetical model of how insulin secretion is regulated. The most important event is the depolarization of the B-cell which causes Ca"+ influx along L-type Ca2+ channels and subsequent increase in cytosolic Ca"+. Depolarization is produced by nutrient (glucose) metabolism via an increase in B-cell ATP and/or ATP/ADP ratio which closes KAXP channels. Also, sulphonylureas, at a distinct location, close KATP channels. The increase in [Ca2+]j activates CaCaMK. Ca2+ uptake appears to be modulated by nutrient metabolism (redox state of NAD(P)H and GSH). Insulin release in response to depolarization is also modulated by factors affecting PLC and adenylate cyclase. Here, production of IP3 leads to release of stored Ca2+ from the endoplasmic reticiulum. DAG activates PKC whereas cAMP activates PKA. CaMK, PKC and PKA cause protein phosphorylations which finally cause granule movement and exocytosis. But there will also be other effects of phosphorylations related to stimulus-secretion coupling, e.g. a possible interaction with voltage-dependent Ca2+ channels. Fig. 20. Hypothetical model of how insulin secretion is regulated. The most important event is the depolarization of the B-cell which causes Ca"+ influx along L-type Ca2+ channels and subsequent increase in cytosolic Ca"+. Depolarization is produced by nutrient (glucose) metabolism via an increase in B-cell ATP and/or ATP/ADP ratio which closes KAXP channels. Also, sulphonylureas, at a distinct location, close KATP channels. The increase in [Ca2+]j activates CaCaMK. Ca2+ uptake appears to be modulated by nutrient metabolism (redox state of NAD(P)H and GSH). Insulin release in response to depolarization is also modulated by factors affecting PLC and adenylate cyclase. Here, production of IP3 leads to release of stored Ca2+ from the endoplasmic reticiulum. DAG activates PKC whereas cAMP activates PKA. CaMK, PKC and PKA cause protein phosphorylations which finally cause granule movement and exocytosis. But there will also be other effects of phosphorylations related to stimulus-secretion coupling, e.g. a possible interaction with voltage-dependent Ca2+ channels.
Nutritional status. Protein-calorie malnutrition is extremely common in alcoholics. Malnutrition may be due not only to poor intake but also to abnormal nutrient metabolism. Whereas poor nutrition may contribute to the evolution of alcoholic liver disease, adequate nutrition does not prevent its development. In fact, Studies suggest that obesity may be a risk factor. [Pg.1818]

Undernutrition usually results from starvation (inadequate nutrient intake) or altered metabolism (inappropriate use of ingested nutrients). Pure starvation occurs when inadequate amounts of appropriate nutrients are available to support tissue repair or synthesis, and changes can be reversed by adequate feeding. An alteration in nutrient metabolism exists when the cell has altered substrate demands... [Pg.2559]

Peroxisome proliferator-activated receptors are ligand-activated receptors which regulate a number of genes involved in nutrient metabolism and energy homeostasis, and thus have served as drug targets for the treatment of metabolic diseases. Anne Reifel Miller and Alan M. Warshawsky review peroxisome proliferator-activated receptor y modulation for the treatment of type 2 diabetes. [Pg.521]

EXERCISE AND NUTRIENT METABOLISM The Hormone Cascade System Growth Factors... [Pg.533]

QUESTION 1 6.2 Describe two functions concerned with nutrient metabolism for each of the following organs ... [Pg.539]


See other pages where Nutrients metabolized is mentioned: [Pg.37]    [Pg.234]    [Pg.166]    [Pg.354]    [Pg.157]    [Pg.177]    [Pg.537]    [Pg.107]    [Pg.241]    [Pg.258]    [Pg.879]    [Pg.8]    [Pg.19]    [Pg.342]    [Pg.363]    [Pg.5810]    [Pg.2292]    [Pg.182]    [Pg.981]    [Pg.185]    [Pg.92]    [Pg.489]    [Pg.14]    [Pg.369]   
See also in sourсe #XX -- [ Pg.440 ]




SEARCH



Acute phase response-induced alterations in maternal and conceptus nutrient metabolism

Nutrient media, metabolic effects

Nutrient metabolism

Nutrient metabolism

THE DIGESTION AND METABOLISM OF NUTRIENTS

© 2024 chempedia.info