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The purpose of the study was to measure the variation in concentrations of plasma neutral and basic amino acids during the day in subjects fed two Mexican model rural diets, one containing 55% (R55) and the other 70% (R70) of energy as carbohydrates, and two model urban diets with the same two proportions of carbohydrates (U55 and U70). The R55 and R70 diets contained 1.35- and 1.69-fold more fiber than the U55 and U70 diets, respectively. Eight female volunteers were adapted to each of the four diets for 3 d before the day of blood sampling. Protein and energy intakes were adjusted to each subject for a consumption of 1 g protein/kg body wt and 150.7 kJ/kg body wt. Blood samples were withdrawn at 0700, 0930, 1100, 1500, 1900, 2300, and 0300. Only plasma concentrations of alanine changed during the day, dropping significantly (P < 0.05) at 2300 and 0300 with the U70 diet. Urban diets produced significantly higher plasma isoleucine and valine values than did the rural diets at some sampling times. Plasma phenylalanine was significantly higher with the U70 diet at 2300 than with the other three diets. Alanine plasma concentrations were significantly higher with the U55 diet at 1900 and significantly lower with the R55 diet at 0930 with respect to the other diets. Lysine was significantly higher at 0700 with the U70 diet than with the other three diets. No other significant changes were observed. These results show the stability of the plasma amino acid profile despite the consumption of different diets in physiologic proportions. Possibly, some of the changes observed in the plasma amino acids can be explained by the high proportion of dietary fiber in the Mexican rural diets. Am J Clin Nutr 1996;63:335-41.

There is not enough information on the classification of oxalate content in several foods, particularly in ethnic foods, to recommend their consumption in subjects with urolithiasis (UL). The objective of the present study was to generate reliable information on the oxalate content and antioxidant activity in different foods and classify them by very low, low, medium, high and very high oxalate content and antioxidant activity.

Peroxisome proliferator-activated receptors (PPARs) are transcription factors that belong to the superfamily of nuclear hormone receptors and regulate the expression of several genes involved in metabolic processes that are potentially linked to the development of some diseases such as hyperlipidemia, diabetes, and obesity. One type of PPAR, PPAR-α, is a transcription factor that regulates the metabolism of lipids, carbohydrates, and amino acids and is activated by ligands such as polyunsaturated fatty acids and drugs used to treat dyslipidemias. There is evidence that genetic variants within the PPARαgene have been associated with a risk of the development of dyslipidemia and cardiovascular disease by influencing fasting and postprandial lipid concentrations; the gene variants have also been associated with an acceleration of the progression of type 2 diabetes. The interactions between genetic PPARαvariants and the response to dietary factors will help to identify individuals or populations who can benefit from specific dietary recommendations. Interestingly, certain nutritional conditions, such as the prolonged consumption of a protein-restricted diet, can produce long-lasting effects on PPARαgene expression through modifications in the methylation of a specific locus surrounding the PPARαgene. Thus, this review underlines our current knowledge about the important role of PPAR-α as a mediator of the metabolic response to nutritional and environmental factors.

Gut hormones play a key role in the regulation of food intake, energy expenditure, glucose homeostasis, lipid metabolism, and a wide range of metabolic functions in response to food ingestion. These hormones are altered in metabolic diseases, such as obesity and type 2 diabetes, and are thus proposed to be possible targets for the prevention or treatment of these diseases. It is clear that food composition, macronutrients, and other non-nutrient components as well as the physical properties of food not only modulate the secretion of gut peptides but also modulate transcription and enteroendocrine cell differentiation, which ultimately modifies gut hormone response. The specific mechanisms or sensing machinery that respond to the different components of the diet have been studied for many years; however, over the last few years, new molecular genetic techniques have led to important advances, thereby allowing a deeper understanding of these mechanisms. This review addresses the current knowledge regarding enteroendocrine cells and how diet interacts with this machinery to stimulate and regulate the secretion of gut peptides. The potential for diet interventions as a promising strategy for modulating gut hormone responses to food ingestion and, ultimately, preventing or treating metabolic diseases is being emphasized considering that these diseases are currently a public health burden.

Obesity is a risk factor for the development of chronic kidney disease (CKD) and end-stage renal disease. It is not clear whether the adoption of a high-protein diet in obese patients affects renal lipid metabolism or kidney function. Thus the aims of this study were to assess in obese Zucker fa/farats the effects of different types and amounts of dietary protein on the expression of lipogenic and inflammatory genes, as well as renal lipid concentration and biochemical parameters of kidney function. Rats were fed different concentrations of soy protein or casein (20, 30, 45%) for 2 mo. Independent of the type of protein ingested, higher dietary protein intake led to higher serum triglycerides (TG) than rats fed adequate concentrations of protein. Additionally, the soy protein diet significantly increased serum TG compared with the casein diet. However, rats fed soy protein had significantly decreased serum cholesterol concentrations compared with those fed a casein diet. No significant differences in renal TG and cholesterol concentrations were observed between rats fed with either protein diets. Renal expression of sterol-regulatory element binding protein 2 (SREBP-2) and its target gene HMG-CoA reductase was significantly increased as the concentration of dietary protein increased. The highest protein diets were associated with greater expression of proinflammatory cytokines in the kidney, independent of the type of dietary protein. These results indicate that high soy or casein protein diets upregulate the expression of lipogenic and proinflammatory genes in the kidney.

We previously showed that long-term consumption of a soy protein diet (SoyP) reduces renal damage in obese Zucker (ObeseZ) rats by restoring urinary NO2and NO3excretion (UNO2/NO3V), suggesting that nitric oxide (NO) deficiency may contribute to the renal progression observed in this model. In addition, there is compelling evidence that hyperleptinemia produced deleterious effects on the kidney through its interaction with the short leptin receptor (ObRa). This study was designed to evaluate the contribution of the NO/endothelial NO synthase (eNOS) system, renal oxidative stress, and ObRa expression to the renoprotection conferred by the consumption of a SoyP in ObeseZ rats. Ten lean and ten male ObeseZ rats were included. One-half of each group was fed with a 20% SoyP and the other half with a 20% casein protein diet (CasP) over the course of 160 days. eNOS protein levels and phosphorylation, renal lipoperoxidation (rLPO), and antioxidant enzyme activity were assessed. In addition, renal ObRa, TGF-β, and kidney injury molecule (Kim-1) mRNA levels, as well as urinary Kim-1 levels, were measured. Renal injury observed in ObeseZ rats fed with CasP was not associated with changes in eNOS expression or phosphorylation. However, this group did present with increased rLPO, reduced catalase activity, and upregulation of ObRa, TGF-β1, and Kim-1. In contrast, ObeseZ rats fed with a SoyP exhibited a reduction in NOS-Thr495 phosphorylation and rLPO, as well as an enhanced catalase activity. These findings were associated with a significant reduction of ObRa, TGF-β1, and Kim-1 mRNA levels and urinary Kim-1 protein. Our results show that renoprotection by SoyP in ObeseZ rats is in part mediated by increased NO availability secondary to a reduction in eNOS-T495 phosphorylation and oxidative stress, together with a significant reduction in ObRa and TGF-β expression.

AbstractIn recent years, the increase in dietary energy availability and sedentary lifestyles hasincreased the development of obesity. Adipose tissue plays an important role in preventingthe accumulation of lipids in other nonadipose tissues. However, during obesity, adipocytesbecome dysfunctional and, as a consequence, the fatty acids (FA) from adipocytes arereleased mainly into the liver. In the liver, FA are esterified to form triacylglycerols (TG) andthere is also an increase in de novo synthesis of FA due to the hyperinsulinemia presentduring obesity. As a result, an accumulation of TG in the liver occurs, resulting in hepaticsteatosis. Lipotoxicity refers to the FA that exceed the capacity of nonadipose tissues tooxidize them, thus enhancing the metabolic flux of FA to form harmful products involved inthe progression of hepatic steatosis to hepatic fibrosis and cirrhosis. As an integral strategyto prevent or treat the consequences of lipotoxicity in humans, healthcare professionalsmust consider new approaches, including type of diet, risk factors, genetic predisposition,treatment/management and prevention.

The purpose of this work was to study whether rat lactating mammary gland can synthesize PUFAs through the expression of Δ5 and Δ6 desaturases (Δ5D and Δ6D), whether these enzymes are regulated by the transcription factors sterol-regulatory element binding protein 1 (SREBP-1) and peroxisome proliferator-activated receptor α (PPARα) and the coactivator peroxisome proliferator-activated receptor γ coactivator 1{szligbeta} (PGC-1{szligbeta}), and whether these desaturases are regulated by the lipid concentration in the diet. The results showed that on day 12 of lactation, ∼35% of the linoleic acid in the diet, which is the precursor of PUFAs, is transferred to the mammary gland. There was expression of Δ5D and Δ6D in mammary gland, and it was regulated by the corn oil content in the diet. The higher the corn oil content in the diet, the lower the expression of both desaturases. Induction of Δ5D and Δ6D was associated positively with similar changes in SREBP-1 and PGC-1{szligbeta}. Expression of PPARα was barely detected and was not affected by the corn oil content in the diet, whereas PGC-1{szligbeta} expression increased as the corn oil in the diet increased. These results indicate that the lactating mammary gland has the capacity to synthesize PUFAs and can be regulated by the lipid content in the diet.

The obese Zucker rat is a valuable model for studying kidney disease associated with obesity and diabetes. Previous studies have shown that substitution of animal protein with soy ameliorates the progression of renal disease. To explore the participation of nitric oxide (NO) and caveolin-1 in this protective effect, we evaluated proteinuria, creatinine clearance, renal structural lesions, nitrites and nitrates urinary excretion (UNO2−/NO3V), and mRNA and protein levels of neuronal NO synthase (nNOS), endothelial NOS (eNOS), and caveolin-1 in lean and fatty Zucker rats fed with 20% casein or soy protein diet. After 160 days of feeding with casein, fatty Zucker rats developed renal insufficiency, progressive proteinuria, and renal structural lesions; these alterations were associated with an important fall of UNO2−/NO3V, changes in nNOS and eNOS mRNA levels, together with increased amount of eNOS and caveolin-1 present in plasma membrane proteins of the kidney. In fatty Zucker rats fed with soy, we observed that soy diet improved renal function, UNO2−/NO3V, and proteinuria and reduced glomerulosclerosis, tubular dilation, intersticial fibrosis, and extracapilar proliferation. Renal protection was associated with reduction of caveolin-1 and eNOS in renal plasma membrane proteins. In conclusion, our results suggest that renal protective effect of soy protein appears to be mediated by improvement of NO generation and pointed out to caveolin-1 overexpression as a potential pathophysiological mechanism in renal disease.

During lactation, the mammary gland has a large demand for amino acids for the synthesis of milk proteins and fatty acids. Arteriovenous differences in amino acids across the mammary gland show an elevated uptake of small neutral amino acids that are mainly transported via system A. The purpose of this study was to characterize the transport of methylaminoisobutyric acid (MeAIB), an amino acid analog used to model transport by system A in lactating rat mammary gland explants. MeAIB accumulation in mammary gland cells increased steadily, and after 3 hours of incubation, the intracellular concentration of the analog was 8-fold higher than the concentration in the medium. MeAIB transport into mammary gland explants showed a Kmof 3.3 ± 0.4 mmol/L and a maximal velocity (Vmax) of 555 ± 23 pmol/μL intracellular fluid (ICF) · min, indicating a system with high capacity but low affinity for its substrate. MeAIB transport into mammary tissue depended highly on Na+, and the uptake was inhibited by addition of natural and analog small neutral amino acids. Cationic, anionic, and large neutral amino acids did not reduce MeAIB transport into mammary gland explants. Preincubation of mammary gland explants in an amino acid—free medium stimulated MeAIB transport, suggesting an adaptive regulation. The addition of an equimolar mixture of alanine, glycine, and serine to the preincubation medium inhibited stimulation of MeAIB transport. Furthermore, stimulation of MeAIB uptake by amino acid starvation was also prevented by the addition of actinomycin D, cycloheximide, tunicamycin, and colchicine. Dibutyryl cyclic adenosine monophosphate (cAMP) increased MeAIB uptake, whereas phorbol 12-myristate 13-acetate (PMA) did not stimulate MeAIB transport. During the first postweaning days, kinetic analyses showed a decrease of 27% in the Vmax. Injection of rat lactating mammary gland mRNA into Xenopus laevisoocytes induced expression of the MeAIB transport system; however, the induction was only 83% above background MeAIB uptake. The results of this study provide a partial explanation for the formation of the metabolic pool of small neutral amino acids in the lactating mammary gland.

ABSTRACTFat and sweeteners contribute to obesity. However, it is unknown whether specific bacteria are selectively modified by different caloric and noncaloric sweeteners with or without a high-fat diet (HFD). Here, we combined extensive host phenotyping and shotgun metagenomics of the gut microbiota to investigate this question. We found that the type of sweetener and its combination with an HFD selectively modified the gut microbiota. Sucralose and steviol glycosides led to the lowest α-diversity of the gut microbiota. Sucralose increased the abundance of B. fragilisin particular, resulting in a decrease in the abundance of occludin and an increase in proinflammatory cytokines, glucose intolerance, fatty acid oxidation and ketone bodies. Sucrose+HFD showed the highest metabolic endotoxemia, weight gain, body fat, total short chain fatty acids (SCFAs), serum TNFα concentration and glucose intolerance. Consumption of sucralose or sucrose resulted in enrichment of the bacterial genes involved in the synthesis of LPS and SCFAs. Notably, brown sugar and honey were associated with the absence of metabolic endotoxemia, increases in bacterial gene diversity and anti-inflammatory markers such as IL-10 and sIgA, the maintenance of glucose tolerance and energy expenditure, similar to the control group, despite the consumption of an HFD. These findings indicate that the type of sweetener and an HFD selectively modify the gut microbiota, bacterial gene enrichment of metabolic pathways involved in LPS and SCFA synthesis, and metabolic endotoxemia associated with different metabolic profiles.