Bitter taste and blood glucose are not involved in the suppressive effect of dietary histidine on food intake.

Histamine decreases food intake by activating histaminergic neurons in the hypothalamus. Histamine is synthesized by histidine decarboxylase (HDC) from histidine. The purpose of this three-part animal study was to clarify the mechanism underlying the suppressive effect of dietary histidine on food intake. In experiment 1, we attempted to distinguish palatability from a direct effect of dietary histidine because histidine tastes slightly bitter to humans. We measured food intake every hour for 24 h in rats fed with a histidine-enriched diet or one of various quinine diets (0.001-0.8% quinine), also bitter. In experiment 2, we measured changes in blood glucose levels in rats fed with a standard or histidine-enriched diet because blood glucose is known to decrease food intake. In experiment 3, we intraperitoneally injected fluoromethylhistidine (FMH), an antagonistic inhibitor of HDC, in rats fed with a histidine-enriched diet. In experiment 1, food intake was almost the same in rats fed with the histidine-enriched diet as that in rats fed with the 0.01% quinine diet until 6 h, but food intake was low in other groups compared with that in the histidine-enriched diet group. After 6 h, food intake did not increase in rats fed with the histidine-enriched diet. In experiment 2, the blood glucose level rose quickly and then began to decrease at approximately 2 h in both groups of rats. However, it decreased more dramatically in rats fed with the histamine-enriched diet and reaches a significant difference from the decrease in the standard-diet group by 6 h. In experiment 3, food intake increased significantly in FMH-injected rats fed with the histidine-enriched diet compared with in non-FMH injected rats. Our results suggest that dietary histidine suppresses food intake by activating histaminergic neurons in the hypothalamus, independently bitter taste and blood glucose level.

Taurine (2-aminoethanesulfonic acid) deficiency creates a vicious circle promoting obesity.

The relation between blood taurine (2-aminoethanesulfonic acid) concentrations and obesity was investigated. Taurine is supplied to the body by dietary ingestion as well as by de novo synthesis; it is anabolized by cysteine dioxygenase (CDO), which is abundantly expressed in liver and white adipose tissue. Overexpression of CDO in 3T3-L1 preadipocytes caused a decrease in the level of cysteine (precursor of taurine) and an increase in the level of taurine in the culture medium, suggesting that CDO is involved in biosynthesis and secretion of taurine in white adipose tissue. In high-fat diet-induced and/or genetically obese mice, a decrease in the blood taurine concentration was observed along with a decrease in CDO expression in adipose tissue but not in liver. Dietary taurine supplementation prevented high-fat diet-induced obesity with increased resting energy expenditure. Thus, taurine deficiency observed in association with obesity may create a vicious circle promoting obesity. Dietary taurine supplementation interrupts this vicious circle and may prevent obesity.

Gender effects in dietary histidine-induced anorexia.

OBJECTIVE: Histamine, a derivative of histidine, decreases food intake by activation of histamine neurons. The aim of the present study was to clarify gender-related differences in food intake through the histidine-histamine neuron system. METHODS: Male, female, and ovariectomized rats were fed a histidine-enriched diet or a control diet with the cafeteria method. RESULTS: The suppressive effect of histidine on food intake was greater in female rats than in male rats, and the suppressive effect of histidine on food intake was less in ovariectomized rats than in female rats. CONCLUSION: Our results indicate that females are more sensitive than males to dietary histidine-induced anorexia.

Histidine supplementation suppresses food intake and fat accumulation in rats.

OBJECTIVE: Histamine, a derivative of histidine, decreases food intake and body fat by activation of histamine neurons. Our objective was to clarify the effect of dietary histidine, in particular, on food intake and/or body fat accumulation in rats. METHODS: Male Wistar rats were assigned to one of four groups after acclimation and allowed free access to diets containing 20% casein (0% histidine), 20% casein plus 1.0% histidine, 20% casein plus 2.5% histidine, or 20% casein plus 5% histidine for 8 d. RESULTS: Food intake and body weight were recorded daily and compared between groups. During the experimental period, food intake decreased according to the increases in dietary histidine. There was a negative and significant (P < 0.01) correlation between dietary histidine (grams per 8 d) and retroperitoneal fat pad (grams per 100 g of body weight). Uncoupling protein-1 mRNA in brown adipose tissue increased with increases in dietary histidine. CONCLUSION: Our results indicate that dietary histidine suppresses food intake and fat accumulation in rats.

Dietary resistant starch alters the characteristics of colonic mucosa and exerts a protective effect on trinitrobenzene sulfonic acid-induced colitis in rats.

The protective effect of a dietary high-amylose cornstarch (HAS) against trinitrobenzene sulfonic acid (TNBS)-induced colitis was examined in rats. Rats were fed a HAS-free basal diet or, a 15% or 30% HAS supplemented diet for 10 d, and then received intracolonic TNBS to induce colitis and fed the respective diets for a further 8 d. HAS ingestion significantly protected colonic injuries as evidenced by lower colonic myeloperoxidase activity. Rats fed the HAS diet showed greater cecal short-chain fatty acid (SCFA) production than those fed the basal diet. Further, just before TNBS administration, HAS ingestion dose-dependently increased fecal and cecal mucin contents, and protein and nucleic acid contents in the colonic mucosa. HAS ingestion also reduced colonic permeability. The protective effect of HAS ingestion on TNBS-induced colitis is perhaps exerted through alterations in colonic mucosa, possibly due to cecal SCFA production.

Physiological functions of resistant proteins: proteins and peptides regulating large bowel fermentation of indigestible polysaccharide.

Animal studies have shown conclusively that feeding of resistant starch (RS) increases production of large bowel total short-chain fatty acids (SCFAs). However, fermentation products of RS may be affected considerably by other dietary ingredients. In rats fed a 20% high-amylose cornstarch (HAS) with casein as the sole protein source, greater cecal SCFAs production was observed compared with that in rats fed a regular cornstarch diet. However, with this diet, the cecal succinate production was also very high. In contrast, when rice or potato protein with lower digestibility was used in place of casein, cecal succinate production decreased with a concomitant increase in butyrate. These observations suggest that nondigested protein, namely resistant protein, might play a role in correcting an imbalance in the ratio of carbohydrate and nitrogen as fermentative substrates for cecal bacteria and in promoting butyrate production. Epidemiological and biochemical data indicate a possible linkage between the fermentation products of starch (butyrate in particular) and the prevention of colorectal cancer as well as ulcerative colits. Accordingly, a fermentation strategy of RS favoring SCFA production should be established to elucidate the potentially beneficial effects of SCFAs on large bowel physiology.

Increasing the amount of fat in a conjugated linoleic acid-supplemented diet reduces lipodystrophy in mice.

Conjugated linoleic acid (CLA) is a naturally occurring group of dienoic derivatives of linoleic acid found in beef and dairy products. However, when 1 g CLA/100 g diet was given to mice in a low fat diet (4 g fat/100 g diet), they showed a marked decrease in fat mass, but demonstrated symptoms of lipoatrophic diabetes, i.e., marked hepatomegaly and insulin resistance. In this study, to determine whether the decrease in adipose tissue was responsible for these adverse effects, mice were fed different doses of CLA and dietary fat. In Experiment 1, mice were fed different doses of CLA (0, 0.1 and 1 g CLA/100 g diet) in a fixed 4 g fat/100 g diet; in those fed 0.1 g CLA, subcutaneous white adipose tissue (WAT) weight was 48% lower than in mice fed 0 g CLA. The mice fed 0.1 g CLA did not exhibit hepatomegaly and insulin resistance. In Experiment 2, mice were fed for 5 mo different amounts of dietary fat (4, 13 and 34 g fat/100 g diet) in 0 or 1 g CLA/100 g diet; in mice fed 1 g CLA with 34 g fat, retroperitoneal and subcutaneous WAT weights were 76 and 79% lower, respectively, than those of mice fed 0 g CLA with 34 g fat. Mice fed 1 g CLA in the diet with 34 g fat had normal plasma insulin concentrations and a 45% greater liver weight. These data suggested that the percentage of CLA in dietary fat might be a determinant of CLA-mediated lipodystrophy.

Green tea flavonoids inhibit the LDL oxidation in osteogenic disordered rats fed a marginal ascorbic acid in diet.

Osteogenic Disorder Shionogi (ODS) rats can not synthesize ascorbic acid (AA). We have examined the capacity of green tea flavonoids (GTF) to modify low-density lipoprotein (LDL) oxidation in ODS rats with dietary AA restriction. In the first experiment, ODS rats were fed diets containing 300 (AA300 diet) or 0 (AA0 diet) mg AA/kg diets for 20 d. In comparison with the AA300 diet, the AA0 diet significantly decreased the concentrations of plasma AA and alpha-tocopherol in LDL and significantly shortened the lag time of LDL oxidation in vitro. In the second experiment, ODS rats were fed one of the following three diets: the AA300 diet, the diet containing 25 mg AA (AA25, marginal AA)/kg diet (AA25 diet), or the diet containing 25 mg AA + 8 g GTF/kg diet (AA25 + GTF diet) for 20 d. Plasma AA concentration were significantly lower in rats fed AA25 compared with AA300 but not in those fed AA25 + GTF. LDL oxidation lag time was significantly longer in rats fed AA25 + GTF compared with the other two groups. Lag time for LDL oxidation was significantly and positively correlated with LDL alpha-tocopherol (r = 0.6885, P = 0.0191). These results suggest that dietary flavonoids suppress the LDL oxidation through the sparing effect on LDL alpha-tocopherol and/or plasma AA when AA intake is marginal in the ODS rats.