The mechanism of the natriuresis of fasting.

Sigler, Miles H.

doi:10.1172/jci107941

Cited by 78 publications

(39 citation statements)

References 27 publications

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“…However, other studies suggested that NPR3 gene expression is decreased markedly by fasting (Sarzani et al 1995), and therefore, the tissue bioactivity of ANP might be promoted in fasting conditions. Increased ANP bioactivity related to NPR3 expression could be related to increased natriuresis, diuresis, hypotension, and lipolysis under low-calorific diets or fasting conditions (Sigler 1975, Sarzani et al 1995, Dessì-Fulgheri et al 1999, Sengenes et al 2002. ANP also has the switching role in glycolysis from anaerobic to aerobic metabolism (Birkenfeld et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Competitive binding of musclin to natriuretic peptide receptor 3 with atrial natriuretic peptide

Kita¹,

Nishizawa²,

Okuno³

et al. 2009

Journal of Endocrinology

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Musclin is a novel skeletal muscle-derived secretory factor that was isolated by our group. Musclin contains a region homologous to natriuretic peptides (NPs). This study investigated the interaction between musclin and NP receptors (NPRs). Musclin specifically bound to NPR3, but not to NPR1 or NPR2. Musclin and atrial natriuretic peptide (ANP) competed for binding to NPR3. We conducted binding assays using various synthetic musclin peptides and mutant musclin proteins. The first NP-homologous region in musclin ( 88 LDRL 91 ) and the second homologous region ( 117 MDRI 120 ) were responsible cooperatively for high-affinity binding to NPR3. The first NP-homologous region was more importantly associated with binding to NPR3, than the second homologous region. The competitive nature of musclin with ANP for the natriuretic clearance receptor NPR3 was also confirmed in vivo. We conclude that musclin binds to NPR3 competitively with ANP and may affect ANP concentrations in a local or systemic manner.

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Section: Discussionmentioning

confidence: 99%

Competitive binding of musclin to natriuretic peptide receptor 3 with atrial natriuretic peptide

Kita¹,

Nishizawa²,

Okuno³

et al. 2009

Journal of Endocrinology

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“…Because the serum albumin remained stable throughout the study, it is unlikely that the remaining 33% of the weight loss was at the expense of the visceral protein pool. Rather, it is probable that a major portion of the nonfat weight loss represents intracellular and extracellular water lost secondary to the natriuresis associated with ketosis (30)(31)(32), as well as water lost in association with the approximately one-third depletion in muscle glycogen stores (normal stores, 500 g, 3 ml of water stored with each g of glycogen, hence 670 g of intracellular contents lost).…”

Section: Discussionmentioning

confidence: 99%

Capacity for Moderate Exercise in Obese Subjects after Adaptation to a Hypocaloric, Ketogenic Diet

Phinney¹,

Horton²,

Sims³

et al. 1980

J. Clin. Invest.

124

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A B S T R A C T To study the capacity for moderate endurance exercise and change in metabolic fuel utilization during adaptation to a ketogenic diet, six moderately obese, untrained subjects were fed a eucaloric, balanced diet (base line) for 2 wk, followed by 6 wk of a protein-supplemented fast (PSF), which provided 1.2 g of protein/kg ideal body wt, supplemented with minerals and vitamins. The mean weight loss was 10.6 kg.The duration of treadmill exercise to subjective exhaustion was 80% of base line after 1 wk of the PSF, but increased to 155% after 6 wk. Despite adjusting up to base line, with a backpack, the subjects' exercise weight after 6 wk of dieting, the final exercise test was performed at a mean of 60% of maximum aerobic capacity, whereas the base-line level was 76%. Resting vastus lateralis glycogen content fell to 57% of base line after 1 wk of the PSF, but rose to 69% after 6 wk, at which time no decrement in muscle glycogen was measured after >4 h ofuphill walking. The respiratory quotient (RQ) during steady-state exercise was 0.76 during base line, and fell progressively to 0.66 after 6 wk of the PSF. Blood glucose was well maintained during exercise in ketosis. The sum of acetoacetate and beta hydroxybutyrate rose from 3.28 to 5.03 mM during exercise after 6 wk of the PSF, explaining in part the low exercise RQ.The low RQ and the fact that blood glucose and muscle glycogen were maintained during exhausting exercise after 6 wk of a PSF suggest that prolonged ketosis results in an adaptation, after which lipid becomes the major metabolic fuel, and net carboThis work was presented in part at the Annual Meeting of the American Federation for Clinical Research, San Francisco, Calif., May 1978. Address reprint requests to Dr. Edward S. Horton, Metabolic Unit, Department of Medicine, University of Vermont, Burlington, Vt. 05405. Received for publication 6 June 1979 and in revised form 21 Table I.Diets. During an initial 2-wk base-line period, the subjects were fed a eucaloric diet providing 1,400 kcal/m2 formulated from common foods, containing 45% of energy as carbohydrate, 40% as fat, and 15% as protein. This diet was sucIAbbreviations used in this paper: PSF, protein-supplemented fast; RQ, respiratory quotient; rT3, 3,3',5'-triiodothyronine; T3, 3,5,3'-triiodothyronine; T4, thyroxine; VO,max, maximum rate of oxygen uptake.ceeded by a 6-wk period during which the subjects ate a diet that consisted of lean meat, fish, or fowl, and provided 1.2 g protein/kg ideal body wt per d. This was supplemented by 25 meq/d of potassium as bicarbonate. Vitamins and iron were supplemented to meet the Recommended Daily Allowance ( Fig. 1). Noncaloric beverages were allowed ad lib. above a mandatory minimum of 1,500 ml/d. Food was salted to taste and extra sodium provided in the form of bouillon when necessary to prevent orthostatic symptoms. Routine monitoring. Weight was measured daily. Blood pressure, pulse, respirations, temperature, and urine ketones (by Acetest tablet, Miles Laboratories, Inc., Elkhart, ...

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“…Lipid catabolism and the (hepatic) production of ketone bodies also increases rapidly and is quantitatively similar after 3 days and 5-6 weeks of starvation (8), but plasma levels increase only gradually to plateau after 4 weeks (4,9). The associated increase in urinary ketone body (organic-acid) excretion requires a compensatory increase in ammonia production and urinary excretion (4,7,10), which is met by an increased renal amino acid uptake and gluconeogenesis (5,6). As a result, the kidney and the liver produce similar amounts of glucose (4,6) and ammonia/urea (7) after 2-3 weeks of fasting.…”

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confidence: 99%

Interorgan Coordination of the Murine Adaptive Response to Fasting

Hakvoort

Moerland

Frijters

et al. 2011

Journal of Biological Chemistry

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Starvation elicits a complex adaptive response in an organism.No information on transcriptional regulation of metabolic adaptations is available. We, therefore, studied the gene expression profiles of brain, small intestine, kidney, liver, and skeletal muscle in mice that were subjected to 0 -72 h of fasting. Functional-category enrichment, text mining, and network analyses were employed to scrutinize the overall adaptation, aiming to identify responsive pathways, processes, and networks, and their regulation. The observed transcriptomics response did not follow the accepted "carbohydrate-lipid-protein" succession of expenditure of energy substrates. Instead, these processes were activated simultaneously in different organs during the entire period. The most prominent changes occurred in lipid and steroid metabolism, especially in the liver and kidney. They were accompanied by suppression of the immune response and cell turnover, particularly in the small intestine, and by increased proteolysis in the muscle. The brain was extremely well protected from the sequels of starvation. 60% of the identified overconnected transcription factors were organ-specific, 6% were common for 4 organs, with nuclear receptors as protagonists, accounting for almost 40% of all transcriptional regulators during fasting. The common transcription factors were PPAR␣, HNF4␣, GCR␣, AR (androgen receptor), SREBP1 and -2, FOXOs, EGR1, c-JUN, c-MYC, SP1, YY1, and ETS1. Our data strongly suggest that the control of metabolism in four metabolically active organs is exerted by transcription factors that are activated by nutrient signals and serves, at least partly, to prevent irreversible brain damage.Adapting to starvation requires an interorgan integration of the activity of metabolic pathways to protect the body from an irreversible loss of resources (1, 2), but how the organism integrates these reactions remains largely unknown. Numerous studies on humans, who fasted for 3-6 weeks, have shown that glycogen stores are depleted within a day (3). The decline in circulating glucose and insulin during the next few days (4) induces a transient increase in plasma (essential) amino acids and a concomitant decline in plasma alanine levels due to an increased hepatic extraction for gluconeogenesis (5, 6). Muscle catabolism is a major source of amino acids in this phase. When fasting is continued, muscle protein catabolism declines, and hepatic uptake of amino acids decreases, which is reflected in a decline of endogenous glucose production (6) and urinary nitrogen excretion (4, 7). Lipid catabolism and the (hepatic) production of ketone bodies also increases rapidly and is quantitatively similar after 3 days and 5-6 weeks of starvation (8), but plasma levels increase only gradually to plateau after 4 weeks (4, 9). The associated increase in urinary ketone body (organic-acid) excretion requires a compensatory increase in ammonia production and urinary excretion (4, 7, 10), which is met by an increased renal amino acid uptake and gluconeogenesis (5, 6)...

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The mechanism of the natriuresis of fasting.

Cited by 78 publications

References 27 publications

Competitive binding of musclin to natriuretic peptide receptor 3 with atrial natriuretic peptide

Competitive binding of musclin to natriuretic peptide receptor 3 with atrial natriuretic peptide

Capacity for Moderate Exercise in Obese Subjects after Adaptation to a Hypocaloric, Ketogenic Diet

Interorgan Coordination of the Murine Adaptive Response to Fasting

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