Organic potassium salts or fibers effects on mineral balance and digestive fermentations in rats adapted to an acidogenic diet

Summary Background Fibers and potassium (K) organic salts in plant foods are liable to affect Ca and Mg balance at digestive and renal levels, respectively. K organic salts could counteract the acidifying effects of western diets and consequences of excess NaCl. Aim of the study To study this question, male rats were adapted to a basal acidifying low-K (LK) diet, or to diets supplemented with a fiber mix (LK/F), or K citrate (HK) or both (HK/F). Results HK and HK/F diets displayed a marked alkalinizing effect in urine and promoted citraturia, but this effect was not modulated by fibers. The effect of fibers on Ca digestive absorption was more potent than K citrate effect on Ca renal excretion. In contrast, K citrate effect on kidney Mg excretion was more effective than that of fibers on Mg digestive absorption, a maximal effect on Mg balance was observed in rats fed the HK/F diet. Digestive fermentations in rats fed the LK/F diet were characterized by high-propionic acid fermentations and succinate accumulation. In rats adapted to the HK/F diet, K citrate supplementation depressed succinate and increased butyrate concentrations. Conclusion Organic anions arising from digestive fermentations seem to be not directly involved in the alkalinizing effects of plant foods. Fibers and organic K salts exert distinct effects on Ca and Mg metabolism, but with interesting interactions as to Mg balance, digestive fermentations and urine pH.     

Effect of potato on acid-base and mineral homeostasis in rats fed a high-sodium chloride diet

Excessive dietary NaCl in association with a paucity of plant foods, major sources of K alkaline salts, is a common feature in Western eating habits which may lead to acid-base disorders and to Ca and Mg wasting. In this context, to evaluate the effects of potato, rich in potassium citrate, on acid-base homeostasis and mineral retention, Wistar rats were fed wheat starch (WS) or cooked potato (CP) diets with a low (0.5 %) or a high (2 %) NaCl content during 3 weeks. The replacement of WS by CP in the diets resulted in a significant urinary alkalinisation (pH from 5.5 to 7.3) parallel to a rise in citrate and K excretion. Urinary Ca and Mg elimination represented respectively 17 and 62 % of the daily absorbed mineral in rats fed the high-salt WS diet compared with 5 and 28 % in rats fed the high-salt CP diet. The total SCFA concentration in the caecum was 3-fold higher in rats fed the CP diets compared with rats fed the WS diets, and it led to a significant rise in Ca and Mg intestinal absorption (Ca from 39 to 56 %; Mg from 37 to 60 %). The present model of low-grade metabolic acidosis indicates that CP may be effective in alkalinising urine, enhancing citrate excretion and ameliorating Ca and Mg balance.     

Effect of potassium salts in rats adapted to an acidogenic high-sulfur amino acid diet

Low-grade metabolic acidosis, consecutive to excessive catabolism of sulfur amino acids and a high dietary Na:K ratio, is a common feature of Western food habits. This metabolic alteration may exert various adverse physiological effects, especially on bone, muscle and kidneys. To assess the actual effects of various K salts, a model of the Westernised diet has been developed in rats: slight protein excess (20 % casein); cations provided as non-alkalinising salts; high Na:K ratio. This diet resulted in acidic urine (pH 5.5) together with a high rate of divalent cation excretion in urine, especially Mg. Compared with controls, K supplementation as KCl accentuated Ca excretion, whereas potassium bicarbonate or malate reduced Mg and Ca excretion and alkalinised urine pH (up to 8). In parallel, citraturia was strongly increased, together with 2-ketoglutarate excretion, by potassium bicarbonate or malate in the diet. Basal sulfate excretion, in the range of 1 mmol/d, was slightly enhanced in rats fed the potassium malate diet. The present model of low-grade metabolic acidosis indicates that potassium malate may be as effective as KHCO3 to counteract urine acidification, to limit divalent cation excretion and to ensure high citrate concentration in urine.     

Protective effects of high dietary potassium: nutritional and metabolic aspects

Potassium (K+) requirements have been largely overlooked because severe deficiencies are uncommon due to the ubiquity of this element in foods. However, a transition toward modern ("Westernized") diets has led to a substantial decline of K+ intake compared with traditional food habits, and a large fraction of the population might now have suboptimal K+ intake. A high K+ intake was demonstrated to have protective effects against several pathologic states affecting the cardiovascular system, kidneys, and bones. Additionally, fruits and vegetables contain K/organic anion salts (malate, citrate), which exert alkalinizing effects, through KHCO(3)(-) generation, which serves to neutralize fixed acidity in urine. Low-grade metabolic acidosis, when not properly controlled, may exacerbate various catabolic processes (bone Ca++ mobilization, proteolysis), especially in the elderly. Fruits and vegetables are therefore receiving great attention in a strategy to increase the nutritional value of meals while reducing energy density and intake. The need to ensure a 2.5- to 3.5-g daily K+ supply from fruits and vegetables represents a strong rationale for the "5-10 servings per day" recommendations.     

Sodium, potassium and chloride utilization by rats given various inorganic anions.

The purpose of the present studies was to examine the effect of ingestion of sodium and potassium salts of various fixed anions on blood pressure, and to assess interactions among electrolytes. In the first study, Sprague-Dawley rats fed on purified diets supplemented with Na salts of chloride, sulphate, bisulphate, carbonate and bicarbonate for 7 weeks developed higher blood pressures than rats fed on the basal diet. In a second study, rats fed on Na or K salts of HSO4, HCO3 or Cl had higher blood pressures than rats fed on the basal diet. Blood pressure measurements were not correlated with plasma volume, plasma renin activity, or plasma atrial natriuretic peptide concentrations at 7 weeks. Plasma renin activity was depressed in rats fed on supplemental Na and even more in rats fed on supplemental K salts rather than the basal diet. Generally, rats fed on supplemental Na excreted Na in urine and absorbed Na in the gut more efficiently than rats fed on the basal diet or diets supplemented with K, but the anions fed also altered Na absorption and excretion. In a third study, rats fed on diets supplemented with any Cl salt, but especially KCl, absorbed K more efficiently than those fed on the basal diet. In studies 1 and 2, the efficiency of urinary excretion of K was greatest when HCO3 and CO3 salts were fed and least when HSO4 salts were fed. Despite large variations in the efficiency of absorption and excretion of Na and K, tissue levels of the electrolytes remained constant.     

Comparison of various phosphate salts as the dietary phosphorus source on nephrocalcinosis and kidney function in rats

The effects of various phosphate salts as the dietary phosphorus sources on the development of nephrocalcinosis and kidney function were examined in rats fed diets containing monophosphate salts (sodium dihydrogenphosphate, NaH2PO4, or potassium dihydrogenphosphate, KH2PO4) or polyphosphate salts (sodium tripolyphosphate, Na5P3O10, or potassium tripolyphosphate, K5P3O10), at levels representing normal phosphorus (normal phosphorus diet) or high phosphorus (high phosphorus diet) contents for 21 d. High phosphorus diet-feeding increased the kidney calcium and phosphorus concentrations. Kidney calcium and phosphorus concentrations were higher in rats fed the high phosphorus diet containing Na5P3O10 or K5P3O10 than in rats fed the high phosphorus diet containing NaH2PO4 or KH2PO4. Nephrocalcinosis was observed in all rats fed a high phosphorus diet, and the degree of nephrocalcinosis was more severe in rats fed Na5P3O10 or K5P3O10 than in rats fed NaH2PO4 or KH2PO4. In rats fed the high phosphorus diet, creatinine clearance was higher in rats fed Na5P3O10 or K5P3O10 than in rats fed NaH2PO4 or KH2PO4. In rats fed Na5P3O10 or K5P3O10, urinary albumin excretion and N-acetyl-beta-D-glucosaminidase (NAG) activity in the urine were increased in rats fed the high phosphorus diet. These were higher in rats fed the high phosphorus diet containing Na5P3O10 than in rats fed the high phosphorus diet containing NaH2PO4 or KH2PO4. This study observed that the development of nephrocalcinosis and kidney function in rats fed the high phosphorus diet was influenced by the difference in monophosphate or polyphosphate salts provided as the dietary phosphorus source, while the effects of sodium and potassium salts were not evident. We suggest that the development of nephrocalcinosis and kidney function in rats fed a high phosphorus diet was altered depending on the form of phosphate salts provided as the dietary source of phosphorus. Additionally, the development of nephrocalcinosis and diminished kidney function in rats fed the high phosphorus diet was more severe for polyphosphate salts as compared to monophosphate salts.     

Enhancement of butyrate production in the rat caecocolonic tract by long-term ingestion of resistant potato starch

Some data suggest that the colonic microflora may adapt to produce more butyrate if given time and the proper substrate. To test this hypothesis, we investigated the effect of prolonged feeding of resistant potato starch on butyrate production. Rats were fed on either a low-fibre diet (basal) or the same diet supplemented with 90 g resistant potato starch/kg (PoS) for 0.5, 2 and 6 months. Short-chain fatty acid (SCFA) concentrations were determined in caecal and colonic contents at the end of each ingestion period. Total SCFA concentration increased over time throughout the caecocolonic tract with PoS, but was not modified with the basal diet. While propionate concentration was unchanged, butyrate concentration was highly increased by PoS at each time period in both the caecum and colon. Moreover, the butyrogenic effect of PoS increased over time, and the amount of butyrate was increased 6-fold in the caecum and proximal colon and 3-fold in the distal colon after 6 months compared with 0.5 months. Accordingly, the ratio butyrate:- total SCFA increased over time throughout the caecocolonic tract (12.6 (SE 2.8) v. 28 (SE 1.8)% in the caecum, 10.5 (SE 1.4) v. 26.8 (SE 0.9)% in the proximal colon, and 7.3 (SE 2.4) v. 23.9 (SE 2.7)% in the distal colon at 0.5 v. 6 months respectively), while the proportion of acetate decreased. Neither the proportion nor the concentration of butyrate was modified over time with the basal diet. Butyrate production was thus promoted by long-term ingestion of PoS, from the caecum towards the distal colon, which suggests that a slow adaptive process occurs within the digestive tract in response to a chronic load of indigestible carbohydrates.     

Calcium, magnesium and phosphorus utilization by rats fed sodium and potassium salts of various inorganic anions

We hypothesized that urinary excretion of calcium would be affected by both urinary excretion of acid and of total fixed anions. Calcium, magnesium and phosphorus utilization was examined in rats fed semipurified diets supplemented with approximately 0.4 mol sodium/kg diet or approximately 0.4 mol potassium/kg diet as chloride, sulfate, bisulfate, carbonate or bicarbonate salts in two studies. The ingestion of supplemental fixed anions (chloride, sulfate or bisulfate) increased urinary excretion of calcium, magnesium and phosphorus. It made no difference whether the anions were ingested as sodium or potassium salts. In Study 1, 80% of the variation in urinary calcium excretion could be explained on the basis of urinary excretion of sulfate, ammonia and total anions. In Study 2, 77% of the variation in urinary calcium excretion could be predicted on the basis of urinary excretion of total anions and sulfate. Although bone and plasma calcium concentrations were not responsive to these dietary changes, less magnesium was retained in bones of rats fed any of the supplemental salts.     

Contribution of the digestive tract microflora to amylomaize starch degradation in the rat.

To study in vivo the contribution of the bacterial flora to amylomaize starch degradation in the rat, germ-free and conventional rats were fed on a diet containing either a normal maize starch or an amylomaize starch. In germ-free rats maize starch was almost totally digested in the small intestine, whereas 40% of the ingested amylomaize starch reached the caecum and 30% was excreted, despite the very high endogenous amylase activity. Study by transmission electron microscopy of germ-free caecal contents showed an endocorrosion of the starch granule. In conventional rats, as in germ-free rats, digestibility of maize starch reached 98% in the small intestine, whereas that of amylomaize starch was only 60%. In the caecum of these rats amylomaize starch was fermented, and this led to a decrease in caecal pH and to formation of short-chain fatty acids (SCFA), especially propionate. Comparison between conventional rats fed on maize starch or amylomaize starch showed that caecal SCFA concentrations during a circadian cycle varied in the same way whereas total SCFA and lactic acid concentrations were much higher in rats fed on amylomaize starch. Amylase (EC 3.2.1.1) activity was similar in the caecal contents of conventional rats whatever the ingested starch. It was lower in conventional than in germ-free rats, but no starch granule remained in the caecum of conventional rats. These results showed that bacterial amylase was more efficient at degrading resistant amylomaize starch than endogenous amylase.     

Chicory increases acetate turnover, but not propionate and butyrate peripheral turnovers in rats

Chicory roots are rich in inulin that is degraded into SCFA in the caecum and colon. Whole-body SCFA metabolism was investigated in rats during food deprivation and postprandial states. After 22 h of food deprivation, sixteen rats received an IV injection of radioactive 14C-labelled SCFA. The volume of distribution and the fractional clearance rate of SCFA were 0.25-0.27 litres/kg and 5.4-5.9 %/min, respectively. The half-life in the first extracellular rapidly decaying compartment was between 0.9 and 1.4 min. After 22 h of food deprivation, another seventeen rats received a primed continuous IV infusion of 13C-labelled SCFA for 2 h. Isotope enrichment (13C) of SCFA was determined in peripheral arterial blood by MS. Peripheral acetate, propionate and butyrate turnover rates were 29, 4 and 0.3 micromol/kg per min respectively. Following 4 weeks of treatment with chicory root or control diets, eighteen fed rats received a primed continuous IV infusion of 13C-labelled SCFA for 2 h. Intestinal degradation of dietary chicory lowered caecal pH, enhanced caecal and colonic weights, caecal SCFA concentrations and breath H2.The diet with chicory supplementation enhanced peripheral acetate turnover by 25 % (P = 0.017) concomitant with an increase in plasma acetate concentration. There were no changes in propionate or butyrate turnovers. In conclusion, by setting up a multi-tracer approach to simultaneously assess the turnovers of acetate, propionate and butyrate it was demonstrated that a chronic chicory-rich diet significantly increases peripheral acetate turnover but not that of propionate or butyrate in rats.     

The effects of ispaghula on rat caecal fermentation and stool output.

The colonic fermentation of ispaghula, a mucilage from Plantago ovata composed mainly of arabinoxylans, and its effects on stool output and caecal metabolism were investigated. Four groups of eight rats were fed on a basal diet (45 g non-starch polysaccharides/kg) for 28 d. The diet was then supplemented with ispaghula (g/kg; 0, 5, 15 or 50) for 28 d. Ispaghula increased stool dry weight and apparent wet weight but faecal water-holding capacity (amount of water held per g dry faecal material at 0.2 mPa) was unchanged. The extent of faecal drying in the metabolism cages was measured for rats fed on the basal diet and 50 g ispaghula/kg diet. At the faecal output levels encountered, only an 8% loss of wet weight would be predicted over 24 h and this was independent of diet. Faecal short-chain fatty acid (SCFA) concentration did not change but SCFA output increased. The molar proportion of SCFA as propionic acid increased and faecal pH was reduced. Values from pooled faecal samples suggested that approximately 50% of the ingested ispaghula was excreted by the 50 g ispaghula/kg diet group. Diaminopimelic acid (a constituent of bacterial cells) concentrations fell but output was unchanged indicating no change in bacterial mass. Similar changes were seen in the caecal contents but caecal pH and SCFA were unaffected. Ispaghula increased both caecal and colonic tissue wet weight and colonic length. Our results suggest that ispaghula is partly fermented in the rat caecum and colon, and loses its water-holding capacity. However, it is still an effective stool bulker and acts mainly by increasing faecal water by some unknown mechanism.     

Restoration of the integrity of rat caeco-colonic mucosa by resistant starch,but not by fructo-oligosaccharides,in dextran sulfate sodium-induced experimental colitis

Butyrate is recognised as efficient in healing colonic inflammation, but cannot be used as a long-term treatment. Dietary fibre that produces a high-butyrate level when fermented represents a promising alternative. We hypothesised that different types of dietary fibre do not have the same efficiency of healing and that this could be correlated to their fermentation characteristics. We compared short-chain fructo-oligosaccharides (FOS) and type 3 resistant starch (RS) in a previously described dextran sulfate sodium (DSS)-induced colitis model. Seventy-two Sprague-Dawley rats received water (control rats) or DSS (50 g DSS/l for 7 d then 30 g DSS/l for 7 (day 7) or 14 (day 14) d). The rats were fed a basal diet (BD), or a FOS or RS diet creating six groups: BD-control, BD-DSS, FOS-control, FOS-DSS, RS-control and RS-DSS. Caeco-colonic inflammatory injuries were assessed macroscopically and histologically. Short-chain fatty acids (SCFA) were quantified in caeco-colon, portal vein and abdominal aorta. At days 7 and 14, caecal and distal macroscopic and histological observations were improved in RS-DSS compared with BD-DSS and also with FOS-DSS rats. Caeco-colonic SCFA were reduced in FOS-DSS and RS-DSS groups compared with healthy controls. The amount of butyrate was higher in the caecum of the RS-DSS rats than in the BD-DSS and FOS-DSS rats, whereas distal butyrate was higher in FOS-DSS rats. Partially explained by higher luminal levels of SCFA, especially butyrate, the healing effect of RS confirms the involvement of some types of dietary fibre in inflammatory bowel disease. Moreover, the ineffectiveness of FOS underlines the importance of the type of dietary substrate.     

Short-chain fatty acid formation in the hindgut of rats fed native and fermented oat fibre concentrates

The formation of SCFA in rats fed fermented oat fibre concentrates was compared with that of rats fed native oat fibre concentrate. The cultures used were lactic acid bacteria consisting of Lactobacillus bulgaricus and Streptococcus thermophilus (V2), the exopolysaccharide-producing strain Pediococcus damnosus 2.6 (Pd) and L. reuteri (Lr). The materials were incorporated into test diets yielding a concentration of indigestible carbohydrates of 80 g/kg (dry weight). Rats fed the V2-fermented fibre-concentrate diet yielded higher caecal and distal concentrations of acetic acid (P < 0.01) than rats fed the native fibre concentrate. All the fermented fibre concentrates resulted in a higher propionic acid concentration in the distal colon (P < 0.05), while rats fed Pd-fermented fibre concentrate resulted in lower concentration of butyric acid (P < 0.05, P < 0.01) in all parts of the hindgut as compared with rats fed the native fibre concentrates. Butyrate concentrations ranged between 5-11 micromol/g (distal colon) and 6-8 micromol/g (13 d faeces). Higher proportions of acetic acid (P < 0.05; P < 0.01) were observed in the caecum of rats fed the fermented fibre concentrates. Rats fed Pd- and Lr-fermented fibre concentrates produced higher proportions of propionic acid (P < 0.05; P < 0.01) in the caecum. Changes in SCFA formation in the caecum, distal colon and faeces of rats fed the fermented samples compared with the native sample indicate that these microbes probably survive in the hindgut and that modification of the microflora composition with fermented foods is possible. This may be important for the gastrointestinal flora balance in relation to colonic diseases.     

Short-chain fatty acids suppress cholesterol synthesis in rat liver and intestine

We previously showed that plasma cholesterol levels decreased following ingestion of a short-chain fatty acid (SCFA) mixture composed of sodium salts of acetic, propionic, and butyric acids simulating cecal fermentation products of sugar-beet fiber (SBF). In the present study, we investigated whether hepatic and small intestinal cholesterol synthesis is involved in the cholesterol-lowering effects of SCFA and SBF. In vitro (expt. 1) and in vivo (expt. 2) cholesterol synthesis rates and the diurnal pattern of SCFA concentrations in portal plasma (expt. 3) were studied in three separate experiments in rats fed diets containing the SCFA mixture, SBF (100 g/kg diet), or the fiber-free control diet. Cholesterol synthesis was measured using 3H2O as a tracer. The in vitro rate of cholesterol synthesis, measured using liver slices, was greater in the SBF group, but not in the SCFA group, than in the fiber-free control group. In contrast, the hepatic cholesterol synthesis rate in vivo was lower in the SCFA group, but not in the SBF group, than in the control group. The mucosal cholesterol synthesis rate for the whole small intestine was <50% of the hepatic rate. The rate in the proximal region was slightly but significantly lower in the SCFA group, and was significantly higher in the SBF group than in the fiber-free group. The rate in the distal small intestines was also significantly greater in the SBF group than in the fiber-free group. Plasma total cholesterol concentrations were lower in the SCFA and SBF groups than in the fiber-free group in both experiments 2 and 3. Diurnal changes in portal SCFA and cholesterol levels were studied in the experiment 3. SCFA concentrations increased rapidly after the start of feeding the SCFA diet, and changes in plasma cholesterol were the reciprocal of those observed in SCFA. These results show that a decrease in hepatic cholesterol synthesis rate mainly contributes to the lowering of plasma cholesterol in rats fed the SCFA mixture diet. Changes in portal SCFA and cholesterol concentrations support this conclusion. In SBF-fed rats, SCFA produced by cecal fermentation are possibly involved in lowering plasma cholesterol levels by negating the counteractive induction of hepatic cholesterol synthesis caused by an increase in bile acid excretion.     

Consumption of raw potato starch increases colon length and fecal excretion of purine bases in growing pigs

Male growing pigs were fed a diet containing 250 g/kg of native corn starch (CS; 26% amylose, 74% amylopectin) or 250 g/kg of raw potato starch (RPS), as examples of digestible starch and resistant starch (Type II), respectively. Whole-tract digestibilities of organic matter, crude protein and starch were greater in pigs fed CS than in those fed RPS through at least d 23 of the study. However, the values progressively increased in the RPS-fed pigs up to d 38, at which time the groups did not differ in organic matter and starch digestibility. The digestive tract and colonic digesta were heavier and colon length longer in pigs fed the RPS diet. Digestibility of starch in the ileum on d 38 was significantly lower in RPS-fed pigs, but rose from ileum to rectum; most starch was extensively fermented in the cecum and proximal colon. Purine base (PB) and short-chain fatty acid (SCFA) concentrations in feces initially increased and then decreased beginning on d 4 for PB and on d 21 for SCFA. PB concentration in feces was greater in pigs fed RPS than in those fed CS. In the large bowel digesta, PB and SCFA concentrations increased from the ileum to the cecum and proximal colon and then fell in the distal colon. Pigs fed the RPS diet had a higher PB concentration in the middle colonic digesta and a greater SCFA concentration in the proximal colonic digesta than the CS-fed group. Adaptation of growing pigs to supplementary RPS required 5 wk, as reflected by whole-tract digestibility and PB and SCFA fecal excretion data.     

Butyrylated starch is less susceptible to enzymic hydrolysis and increases large-bowel butyrate more than high-amylose maize starch in the rat

Large-bowel fermentation of resistant starch produces SCFA that are believed to be important in maintaining visceral function. High-amylose maize starch (HAMS) and acylated starches are sources of resistant starch and are an effective means of increasing colonic SCFA. Cooking increases digestibility of starches but its effects on the capacity of these starches to raise large-bowel SCFA are unknown. We have examined the effects of cooking of HAMS and butyrylated HAMS (HAMSB) on amylolysis in vitro and their capacity to raise caeco-colonic SCFA in rats. The starches were boiled in excess water and microwaved, followed by drying at 100 degrees C. Cooking increased in vitro glucose release for both starches but significantly less from HAMSB. Rat growth rates were unaffected when fed cooked resistant starch. Digesta pH was increased in the caecum and proximal colon of rats fed cooked HAMS. Distal colonic pH was highest in rats fed cooked HAMSB. Factorial analyses (2x2) of caecal SCFA pools showed significant differences between HAMS and HAMSB, and that cooking significantly lowered caecal butyrate pools. Portal venous butyrate concentrations were higher in both HAMSB groups than those fed HAMS. The data suggest that HAMSB is less susceptible to in vitro amylolysis than HAMS following cooking and delivers more butyrate to rat caecum than HAMS. This attribute may be useful in food applications for specific delivery of SCFA to the colon. Preparation of carbohydrates to simulate human food in animal experiments may be important to assess nutritional and physiological effects accurately.     

Diet, evolution and aging

Theoretically, we humans should be better adapted physiologically to the diet our ancestors were exposed to during millions of years of hominid evolution than to the diet we have been eating since the agricultural revolution a mere 10,000 years ago, and since industrialization only 200 years ago. Among the many health problems resulting from this mismatch between our genetically determined nutritional requirements and our current diet, some might be a consequence in part of the deficiency of potassium alkali salts (K-base), which are amply present in the plant foods that our ancestors ate in abundance, and the exchange of those salts for sodium chloride (NaCl), which has been incorporated copiously into the contemporary diet, which at the same time is meager in K-base-rich plant foods. Deficiency of K-base in the diet increases the net systemic acid load imposed by the diet. We know that clinically-recognized chronic metabolic acidosis has deleterious effects on the body, including growth retardation in children, decreased muscle and bone mass in adults, and kidney stone formation, and that correction of acidosis can ameliorate those conditions. Is it possible that a lifetime of eating diets that deliver evolutionarily superphysiologic loads of acid to the body contribute to the decrease in bone and muscle mass, and growth hormone secretion, which occur normally with age? That is, are contemporary humans suffering from the consequences of chronic, diet-induced low-grade systemic metabolic acidosis? Our group has shown that contemporary net acid-producing diets do indeed characteristically produce a low-grade systemic metabolic acidosis in otherwise healthy adult subjects, and that the degree of acidosis increases with age, in relation to the normally occurring age-related decline in renal functional capacity. We also found that neutralization of the diet net acid load with dietary supplements of potassium bicarbonate (KHCO3) improved calcium and phosphorus balances, reduced bone resorption rates, improved nitrogen balance, and mitigated the normally occurring age-related decline in growth hormone secretion--all without restricting dietary NaCl. Moreover, we found that co-administration of an alkalinizing salt of potassium (potassium citrate) with NaCl prevented NaCl from increasing urinary calcium excretion and bone resorption, as occurred with NaCl administration alone. Earlier studies estimated dietary acid load from the amount of animal protein in the diet, inasmuch as protein metabolism yields sulfuric acid as an end-product. In cross-cultural epidemiologic studies, Abelow found that hip fracture incidence in older women correlated with animal protein intake, and they suggested a causal relation to the acid load from protein. Those studies did not consider the effect of potential sources of base in the diet. We considered that estimating the net acid load of the diet (i. e., acid minus base) would require considering also the intake of plant foods, many of which are rich sources of K-base, or more precisely base precursors, substances like organic anions that the body metabolizes to bicarbonate. In following up the findings of Abelow et al., we found that plant food intake tended to be protective against hip fracture, and that hip fracture incidence among countries correlated inversely with the ratio of plant-to-animal food intake. These findings were confirmed in a more homogeneous population of white elderly women residents of the U.S. These findings support affirmative answers to the questions we asked above. Can we provide dietary guidelines for controlling dietary net acid loads to minimize or eliminate diet-induced and age-amplified chronic low-grade metabolic acidosis and its pathophysiological sequelae. We discuss the use of algorithms to predict the diet net acid and provide nutritionists and clinicians with relatively simple and reliable methods for determining and controlling the net acid load of the diet. A more difficult question is what level of acidosis is acceptable. We argue that any level of acidosis may be unacceptable from an evolutionarily perspective, and indeed, that a low-grade metabolic alkalosis may be the optimal acid-base state for humans.     

Megasphaera elsdenii JCM1772T normalizes hyperlactate production in the large intestine of fructooligosaccharide-fed rats by stimulating butyrate production

Hyperlactate production is related to disorders of the large intestine such as inflammatory bowel diseases. Lactate, an intermediate in hindgut fermentation, is metabolized to SCFA. Megasphaera elsdenii can convert lactate to butyrate, a physiologically important organic acid for the hindgut mucosa. This experiment was conducted to determine whether M. elsdenii normalizes hyperlactate production and stimulates butyrate production in the rat large intestine. Specific pathogen-free Sprague-Dawley male rats (n = 12) were fed a fructooligosaccharide (FOS)-supplemented (100 g/kg), semipurified diet to induce lactate production. Lactate excretion in all rats was >30 mmol/kg fresh feces on d 2 of FOS-feeding. The rats were divided into two groups on the morning of d 4. One group (n = 5) was dosed orally with M. elsdenii JCM1772T (1.3 x 10(13) cells) for 3 d. The other group was treated with a vehicle solution. Fecal lactate was significantly lower in rats administered M. elsdenii than in controls. An increase in fecal butyrate compensated for the decrease in lactate. The number of cecal epithelial cells was greater in rats administered M. elsdenii than in controls. M. elsdenii has the potential to normalize hyperlactate accumulation in the large intestine, and lactate-utilizing butyrate producers may be useful probiotics when hyperlactate fermentation in the large intestine is a problem.     

Gastrointestinal implications in pigs of wheat and oat fractions. 2. Microbial activity in the gastrointestinal tract.

The present work was undertaken to study the microbial activity in various segments of the gastrointestinal (GI) tract of pigs as influenced by the source and level of wheat and oat dietary fibre (DF). Eight experimental diets were prepared from wheat and oat fractions and studied in a series of two experiments using wheat flour as the DF-depleted control. The diets in Expt 1 were based on wheat flour and three iso-DF enriched diets comprising fractions rich in wheat aleurone, pericarp/testa or bran. In Expt 2, oat bran was added to wheat flour to achieve the same DF intake level as in Expt 1. This series included further diets based on rolled oats and rolled oats plus oat bran. The eight diets were given to thirty-two ileal-cannulated pigs, with sixteen pigs in each experiment. After a total period of 34 d (Expt 1) and 42 d (Expt 2), the pigs were slaughtered 4 h post-feeding and samples taken for adenine nucleotides (adenosine 5'-triphosphate (ATP); adenylate energy charge (AEC)), organic acids (lactic acid (LA); short chain fatty acids (SCFA)) and pH at twelve sites of the GI tract. The microbial activity as measured by the ATP concentration was low in the stomach and the cranial two-thirds of the small intestine, but tended to increase in the distal third. In the caecum a sharp rise in microbial activity was observed; the highest level was found for the diet providing most fermentable substrates. In all the diets but the rolled oats + oat bran diets, microbial activity showed a descending pattern as the digesta moved through the colon. In the large intestine source and level of residues had a marked influence on microbial activity. LA was the chief organic acid in the stomach and small intestine (10-40 mmol/l) while LA relative to SCFA was a minor component in the caecum and colon (10-20 mmol/l). The contribution of SCFA to total organic acids was reciprocal to LA, i.e. low in the stomach and small intestine (less than 20 mmol/l) and high in the caecum and colon. In the large intestine the concentration of SCFA decreased from 100-140 mmol/l in the caecum and proximal colon to 40-80 mmol/l in the distal colon. The acetic: propionic acid ratio increased from the caecum to the distal colon. With the diets based on oat alone (rolled oats; rolled oats + oat bran) the increase was less significant.(ABSTRACT TRUNCATED AT 400 WORDS)     

The influence of creatinine, lecithin and choline feeding on aliphatic amine production and excretion in the rat

The excretion of aliphatic amines, methylamine, dimethylamine and trimethylamine in the urine and faeces of rats fed on a control diet and diets supplemented with creatinine, lecithin or choline were measured over a 14 d feeding period. The rats were then killed and concentrations of amines in small and large intestinal contents measured. Adding creatinine to the diet resulted in a significant increase of methylamine excretion in the faeces and urine. The amount of methylamine found in all parts of the intestine increased, especially in the caecum. Adding lecithin to the diet resulted in an increase in the methylamine excretion only, and no change in the concentrations of amines found in the intestine, except for trimethylamine which was significantly increased in the caecum and colon. Adding choline to the diet resulted in a significant increase in excretion of trimethylamine and, to a lesser extent, methylamine. The levels of amines found in the gut increased, dimethylamine being increased in the small bowel, and methylamine and trimethylamine in the caecum.