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Liquid versus solid carbohydrate: effects on food intake and body weight.

BACKGROUND: Beverages are contributing an increased proportion of energy to the diet. Because they elicit a weak compensatory dietary response, they may increase risk of positive energy balance. OBJECTIVES: This study aimed to document the differential effects of matched liquid and solid carbohydrate loads on diet and body weight. DESIGN: In a cross-over design, seven males and eight females consumed dietary carbohydrate loads of 1880 kJ/day as a liquid (soda) or solid (jelly beans) during two 4 week periods separated by a 4 week washout. Subjects were permitted to consume the loads however they chose. In addition to baseline measurements, diet records were obtained on random days throughout the study, body composition was measured weekly, physical activity was assessed before and after treatments and hunger was assessed during washout and midway through each treatment. RESULTS: Free-feeding energy intake during the solid period was significantly lower than intake prior to this period. Dietary energy compensation was precise (118%). No decrease in free-feeding energy intake occurred during the liquid period. Total daily energy intake increased by an amount equal to the load resulting in dietary compensation of -17%. Consequently, body weight and BMI increased significantly only during the liquid period. Physical activity and hunger were unchanged. CONCLUSIONS: This study indicates that liquid carbohydrate promotes positive energy balance, whereas a comparable solid carbohydrate elicits precise dietary compensation. Increased consumption of energy-yielding fluids may promote positive energy balance.

Adult↗

Cytokine profile of serum and bronchoalveolar lavage fluids following thoracic esophageal cancer surgery.

OBJECTIVES: The body's response to stress is comprised of two opposing reactions, namely inflammation and immunosuppression. The balance between these two reactions not only changes over time, but also varies among different cells or organs. Limited information is available regarding the cytokine balance of circulating blood and inflammatory sites after thoracic surgical stress. DESIGN: The subjects of the present study were 10 patients undergoing esophageal cancer surgery which requires thoracolaparotomic manipulation. The postoperative levels of interleukin (IL)-8, IL-10, IL-1 receptor antagonist (IL-1ra) and soluble tumor necrosis factor receptor I (sTNF-RI) in bronchoalveolar lavage fluids (BALFs) and peripheral blood were measured by enzyme-linked immunosorbent assay. The absolute concentration of cytokines in lower respiratory tract ([cytokine](LRT)) was estimated by using the ratio of urea concentration in BALF and serum. RESULTS: The levels of these cytokines in peripheral blood peaked within 24 h of start of the surgery (IL-8 85.6 +/- 29.8 pg/ml; IL-10 65.1 +/- 10.6 pg/ml; IL-1ra 2,807.8 +/- 652.8 pg/ml, and sTNF-RI 3,996.3 +/- 380.1 pg/ml). The level of [IL-8](LRT) immediately after surgery was approximately 20 times higher than that in peripheral blood, and the level of [IL-1ra](LRT) was approximately 4 times higher. In contrast, the level of [IL-10](LRT) immediately after surgery was comparable to that in peripheral blood, but the level of [sTNF RI](LRT) immediately after surgery was approximately one fifth of that in peripheral blood. CONCLUSIONS: The balance between pro- and anti-inflammatory reactions varies from one part of the body to the next, and changes over time after surgery. The profile of stress-induced pro-inflammatory cytokines and anti-inflammatory cytokines should be analyzed further to establish appropriate and effective cytokine modulatory therapeutic approaches.

Aged↗

Plasma, red blood cell, total blood, and extracellular fluid volumes in healthy horse foals during growth.

During the growth interval encompassing age 2 days through 24 weeks, plasma, RBC, total blood, and extracellular fluid (ECF) volumes were determined in 7 healthy, resting foals. Evans blue dye and sodium thiocyanate were used to estimate plasma and ECF volumes, respectively. Absolute plasma volume remained stable from 2 days through 2 weeks of age, then increased progressively through 24 weeks of age. After decreasing between 2 days and 2 weeks of age, absolute RBC and total blood volumes progressively increased. Absolute ECF volume increased progressively from 2 days of age through 24 weeks of age, but plasma, RBC, and total blood volumes decreased relative to body weight increase. During the first 12 weeks of life, ECF volume decreased relative to body weight increase, and then remained stable during the next 12 weeks. There were close correlations between age, as well as body weight, and plasma, RBC, total blood, and ECF volumes. The relationship defined between age and the respective fluid and blood volumes provided a useful tool for evaluation and management of alterations of fluid balance in the foal.

Animals↗

Peptide metabolism and the control of body fluid homeostasis.

In this paper, we review our current understanding of the medicinal chemistry of the major peptide systems, which influence body fluid homeostasis. Electrolytes play pivotal roles in intra- and intercellular communication, acid-base equilibrium and, when bound to several macromolecules, they regulate a myriad of enzymatic proteins, receptors and transcription factors. Cell turgor influences the plasma membrane, which activates mechanically-gated ion channels or mechanoreceptors, and the expression of a number of genes which underlie long-term metabolic responses to hormones, substrates and reactive oxygen intermediates. The altered kinetics and enzymatic cleavage of peptides during water-electrolyte imbalance can contribute to cardiac and renal damage associated with elevated blood pressure. Identification of the enzymes which are responsible for cleavage, together with emerging information about the mechanisms of action and structures of regulatory and effector peptides, has laid a foundation for the discovery of novel drugs, some of which are in use or are now undergoing evaluation in experimental trials. The development of models of hydrosaline challenge with relative efficiency to induce selective water-electrolyte imbalance has permitted the identification of kallikrein-kinin, renin-angiotensin-aldosterone, vasopressin-oxytocin, thyrotropin-releasing hormone and luteinizing hormone-releasing hormone as susceptible substrates. At present, the angiotensin-I converting enzyme inhibitors are well-known efficacious, orally active, blood pressure-lowering agents which have been used in hypertensive patients. In addition to several new analogues of this class of drug, some selective dual inhibitors of angiotensin-I converting enzyme and neutral endopeptidase and inhibitors of aminopeptidases are now also being rationally assayed and their beneficial effects on hypertension and hydromineral balance indicate that this type of drug may have powerful therapeutic effects for disorders of body fluid homeostasis.

Animals↗

Profound pharmacologic inhibition of renal tubule sodium and water reabsorption in rats.

Vanadate, furosemide, chlorothiazide, acetazolamide, and amiloride were infused concomitantly into conscious rats to determine the extent to which renal sodium reabsorption can be inhibited. The animals were maintained in exact fluid balance despite exorbitant urine flow rates by intravenous infusion of an isotonic salt solution sufficient to keep body weight constant. In maximally effective doses vanadate, furosemide, chlorothiazide, acetazolamide, and amiloride increased sodium excretion to an amount equal to 69% of the filtered load. Together with isotonic extracellular fluid expansion equal to 7% of body weight, these pharmacologic agents increased sodium excretion to an amount equal to 83.7% of the filtered load, a level of sustained sodium excretion that has not been reported previously in mammals. These studies demonstrate that tubular sodium and water reabsorption can be profoundly inhibited in vivo by drugs that diminish sodium and water transport in proximal as well as in distal tubules.

Acetazolamide↗

Change in bioelectrical impedance following laparoscopic and open abdominal surgery.

The effect of surgery, and in particular, the relative effects of open and laparoscopic abdominal surgery on whole body bioelectrical impedance (BI) has been investigated. Repeated measurements of BI were performed over a 60 h period in 12 patients undergoing laparoscopic surgery (group A) and in 12 patients undergoing elective open abdominal surgery for benign conditions (group B). Control measurements were performed upon 4 healthy adult subjects over the same time period. Attempts were made to relate postoperative changes in BI in group A and group B to changes in net postoperative fluid balance. The postoperative disturbance in BI was significantly greater in group B than group A (P < 0.001 Mann-Whitney-U test) and differed significantly from the minor fluctuations of BI observed in the control group (P < 0.001 Mann-Whitney-U test). The fluctuations in BI observed after laparoscopic surgery were not significantly greater than those seen in the control group (P = 0.1 Mann- Whitney U test). Changes in BI in both group A and B did not correlate with changes in net postoperative fluid balance, which suggests that the effect of surgery upon BI was related to changes of body water distribution rather than changes in total body water volume.

Journal Article↗

[The Stewart model. "Modern" approach to the interpretation of the acid-base metabolism].

About twenty years ago, Peter Stewart had already published his modern quantitative approach to acid-base chemistry. According to his interpretations, the traditional concepts of the mechanisms behind the changes in acid-base balance are considerably questionable. The main physicochemical principle which must be accomplished in body fluids, is the rule of electroneutrality. There are 3 components in biological fluids which are subject to this principle: a)Water, which is only in minor parts dissociated into H+ and OH-, b)"strong", i.e. completely dissociated, electrolytes, which thus do not interact with other substances, and body substances, such as lactate, and c)"weak", i.e. incompletely dissociated, substances. Peter Stewart strictly distinguished between dependent and independent variables and thus indeed described a new order of acid-base chemistry. The 3 dependent variables (bicarbonate concentration [Bic(-)], pH, and with this also hydrogen ion concentration [H(+)]) can only change if the 3 independent variables allow this change. These 3 independent variables are: 1. Carbon dioxide partial pressure, 2.the total amount of all weak acids ([A-] (Stewart called these ATOT), and 3.strong ion difference (SID). [A(-)] can be calculated from the albumin (Alb) and the phosphate concentration (Pi): [A(-)]=[Alb x (0.123 x pH - 0.631)] + [Pi x (0.309 x pH - 0.469)]. An apparent SID (or "bedside" SID) can be calculated using measurable ion concentrations: SID=[Na(+)] + [K(+)] - [Cl(-)]-lactate. Regarding the metabolic disturbances of acid-base chemistry, according to Stewart's terminology, changes in pH, [H(+)], and [Bic(-)] are only possible if either SID or [A(-)] itself changes. If, for example, SID decreases (e.g. in case of hyperchloremia), this increase in independent negative charges leads to a decrease in dependent negative charges in terms of [Bic(-)] resulting in acidosis (and vice versa). Therefore, according to Stewart, the decrease in SID during hyperchloremic acidosis results from the increase in serum chloride concentration and is the causal mechanism behind this acidosis. Contrary for example, a decrease in [A(-)] (e. g. during hypoalbuminemia) leads to an increase in [Bic(-)] and therefore to an alcalosis (and vice versa). Thus, by Stewart's approach, completely new acid-base disturbances, like "hyperchloremic acidosis" or "hypoalbuminemic alcalosis" (which, of course, can also exist in combination) can be detected, which had been unrecognised by the classic acid-base concepts. Consequently, Stewart's analysis can lead to a better understanding of the mechanisms behind the changes in acid-base balance.

Acid-Base Equilibrium↗

Renal excretion of water in men under hypokinesia and physical exercise with fluid and salt supplementation.

It has been suggested that under hypokinesia (reduced number of steps/day) and intensive physical exercise, the intensification of fluid excretion in men is apparently caused as a result of the inability of the body to retain optimum amounts of water. Thus, to evaluate this hypothesis, studies were performed with the use of fluid and sodium chloride (NaCl) supplements on 12 highly trained physically healthy male volunteers aged 19-24 years under 364 days of hypokinesis (HK) and a set of intensive physical exercises (PE). They were divided into two groups with 6 volunteers per group. The first group of subjects were submitted to HK and took daily fluid and salt supplements in very small doses and the second group of volunteers were subjected to intensive PE and fluid-salt supplements. For the simulation of the hypokinetic effect, both groups of subjects were kept under an average of 4000 steps/day. During the prehypokinetic period of 60 days and under the hypokinetic period of 364 days water consumed and eliminated in urine by the men, water content in blood, plasma volume, rate of glomerular filtration, renal blood flow, osmotic concentration of urine and blood were measured. Under HK, the rate of renal excretion of water increased considerably in both groups. The additional fluid and salt intake failed to normalize water balance adequately under HK and PE. It was concluded that negative water balance evidently resulted not from shortage of water in the diet but from the inability of the body to retain optimum amounts of fluid under HK and a set of intensive PEs.

Adult↗

Cyclic GMP excretion blocked by isatin administration under conditions of fluid overload.

Isatin is a potent inhibitor of atrial natriuretic peptide (ANP) receptors and ANP-induced generation of cGMP in vitro. This study was designed to determine whether it had a similar effect in vivo, using a model of fluid overload known to induce ANP. We confirmed that this model increased urinary output of cGMP 3 hr after volume loading, and showed that this effect was blocked by i.p. injection of isatin (50 mg/kg). Isatin had no effect on urine volume or sodium output. However, isatin did have an effect on plasma protein concentration, both compared with control values, compatible with shifting fluid to the vascular compartment, and after volume overload, in which it normalised such a shift. Isatin thus affected both the generation of cGMP and fluid balance in vivo.

Analysis of Variance↗

Acid-base balance in plasmatic, pericardial and peritoneal fluids in 2 species of amphibians.

The carbonic acid-base balance and the concentrations of Na and Cl were studied in 3 fluids, plasmatic, pericardial and peritoneal, sampled from 2 species of amphibians: Pleurodeles waltl and Xenopus laevis. In Pleurodeles the pericardial and peritoneal fluids are in a state of marked metabolic alkalosis, the carbonate alkalinity being up to 10 times higher in the serosal fluids than in the plasma, whereas PCO2's are very close in the 3 fluids. The Cl concentration is markedly lower in the serosal fluids than in the plasma. In Xenopus, the metabolic alkalosis of the serosal fluids also exists, but to a much lower extent than in Pleurodeles. These observations lead to further researches in the field of morphometry, physicochemistry and physiology.

Acid-Base Equilibrium↗

Compensatory enteral hyperalimentation for management of patients with severe short bowel syndrome.

In order to evaluate the effects of an unrestricted, compensatory, enteral hyperalimentation in patients with short bowel syndrome, we retrospectively selected from 128 consecutive patients with extensive small bowel resection a group of 25 who developed under this regimen a massive protracted diarrhea (fecal weight 2005-6188 g/day). All the patients but one were weaned from parenteral nutrition by the eighth day after admission. Although fecal weight increased in relation to the increase of the enteral intake, there was a significant gain of body weight, serum-albumin, and creatinine-height index and an improved fluid and electrolyte balance through the period of hospitalization. By contrast, 18 of the 25 patients developed hypocalcemia and/or hypomagnesemia. After discharge (median follow-up, three years), most patients resumed normal social activity. It is concluded that exclusively enteral hyperalimentation can stabilize most patients with severe short bowel syndrome even in the case of massive fecal losses.

Adult↗

The renin-angiotensin system. Normal physiology and changes in older hypertensives.

The long-term effects of angiotensin (ANGII) on arterial pressure regulation appear to be closely linked to volume homeostasis, via the renal-pressure natriuresis mechanism, both in normal humans and in older hypertensives. In response to disturbances such as increased sodium intake, suppression of ANGII and aldosterone formation greatly amplifies the effectiveness of the pressure natriuresis mechanism, thereby preventing large increases in body fluid volumes and minimizing the rise in blood pressure needed to maintain sodium balance. When ANGII levels are inappropriately elevated, the antinatriuretic effects of ANGII cause increased arterial pressure, which then serves to maintain sodium and water balance via the pressure natriuresis mechanism. The primary intrarenal and extrarenal mechanisms by which ANGII controls renal excretion and arterial pressure include: (1) a direct effect of ANGII on tubular sodium transport; (2) a preferential constrictor action of ANGII on efferent arterioles, which increases sodium reabsorption by altering peritubular capillary physical forces (efferent arteriolar constriction also prevents excessive decreases in glomerular filtration rate when renal perfusion is compromised, such as in renal artery stenosis); and (3) extrarenal effects of ANGII, including stimulation of aldosterone secretion. Current evidence suggests that the direct effects of ANGII on the kidney are quantitatively more important than indirect effects mediated by aldosterone. In older hypertensives, plasma renin activity and aldosterone concentration are often suppressed, perhaps due to loss of functional nephrons and increased sodium chloride delivery to the macula densa of the remaining nephrons.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

Metabolic and endocrine changes in spinal cord injury: I. The nervous system before and after transection of the spinal cord.

This is the first article of a 4-part series which provides a comprehensive, concise review and analysis of the pertinent literature published over the last 25 years on the metabolic and endocrine consequences of spinal cord injury. This article begins with a brief overview of the physiology of the nervous system, and then reviews the metabolic changes associated with the motor paralysis which follows cervical spinal cord injury. Studies reviewed on SCI patients include investigations of body composition (lean mass, fat, creatinine, water, electrolytes), urine composition (creatinine, uric acid, fluid balance, electrolytes), and the blood flow and histochemistry of paralyzed muscles. Studies reviewed from animal models include investigations of the properties of muscle cells, membranes, somatic receptors, and the kinetics of electrolytes in paralyzed limbs, and how succinylcholine modified these properties and kinetics. Information from articles reviewed here is organized under the following headings: problems studied, methods of investigation and results, conclusions, summary of results, discrepancies, areas of needed research, and practical clinical implications. Highlights of pertinent data contained in the original articles are organized in tables to facilitate direct comparisons between similar studies and between data on healthy and spinal cord injured subjects.

Animals↗

Differential regulation of angiotensinogen and natriuretic peptide mRNAs in rat brain by osmotic stimulation: focus on anterior hypothalamus and supraoptic nucleus.

Central angiotensin II and natriuretic peptide systems have been shown to be involved in the central regulation of blood fluid homeostasis with alterations in central peptide and/or receptor levels observed following changes in osmotic status. The present study investigated the effects of sodium loading on mRNA encoding the angiotensin II precursor, angiotensinogen (AOGEN), and the natriuretic peptides, atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP) in rat brain using quantitative in situ hybridization histochemistry of [35S]- and [33P]-labeled oligonucleotide probes. Following 7 and 14 days of 2% sodium chloride in drinking water a significant increase was detected in preproAOGEN (ppAOGEN) mRNA in presumed astrocytes in regions of the anterior hypothalamus, including the periventricular nucleus, the medial preoptic area and medial preoptic nucleus, while a decrease was observed in astrocytes in the supraoptic nucleus. Other forebrain regions examined including the subfornical organ, bed nucleus of the stria terminalis and the arcuate nucleus showed no significant alteration in the level of ppAOGEN mRNA. Sodium loading did not appreciably alter ppANP or ppCNP mRNA levels in neurons of the anteromedial preoptic or arcuate nuclei or hippocampus at the times studied. PpANP mRNA levels were also unaltered in Barrington's nucleus following sodium loading, while preprocorticotropin-releasing hormone mRNA was significantly decreased. These results indicate that AOGEN mRNA transcription/stability in vivo is modulated by alterations in osmotic balance, consistent with previous reports of a central role for AII in cardiovascular and body fluid homeostasis. In contrast, despite reports of modulation of hypothalamic ANP-immunoreactivity following changes in osmotic status, it would appear that osmotic stimulation over periods of 7-14 days does not markedly alter the transcription or stability of hypothalamic natriuretic peptide mRNAs in vivo.

Angiotensinogen↗