Onset of nephrocalcinosis depends on dietary phosphorus concentration in male rats fed a magnesium-deficient diet.

Although a magnesium (Mg)-deficient diet is generally known to induce nephrocalcinosis, our previous study observed that despite the administration of a Mg-deficient diet, the kidney calcium (Ca) and phosphorus (P) concentrations were not increased in male rats. We speculated that this result was due to the P concentration of the experimental diet based on the AIN-93G formula used in the previous study. In the present study, male rats were fed modified AIN-93G diets containing the two different Mg concentrations [0.5 g per kg diet (normal-Mg) or Mg-free (Mg-deficient)] and three different P concentrations [3 (3-P), 5 (5-P) or 7 (7-P) g per kg diet]. By histological examination of the kidney, nephrocalcinosis was not observed in rats fed on the Mg-deficient diet containing 3-P While nephrocalcinosis appeared in rats fed on the Mg-deficient diet containing 5-P and 7-P The degree of nephrocalcinosis was severe in rats fed on the Mg-deficient diet containing 7-P compared with rats fed on the Mg-deficient diet containing 5-P These results demonstrated that the Mg-deficient diet based on AIN-93G formula dose not induce nephrocalcinosis and that the Mg-deficient diet based on AIN-93G formula with increased dietary P concentrations induces nephrocalcinosis in male rats. We suggest that the onset of nephrocalcinosis could depend on the dietary P concentration in male rats fed on a Mg-deficient diet.     

Dietary fructose produces greater nephrocalcinosis in female than in male magnesium-deficient rats

The synergistic interaction of fructose and magnesium (Mg) deficiency on kidney calcification was compared in male and female rats. Male and female weanling rats were divided into four dietary groups: fructose or starch, with or without Mg. Rats were fed their respective diets for 9 weeks, and 24 h urine was collected to measure urinary output, pH, Mg, calcium (Ca), and oxalic acid. Rats were fasted overnight. After decapitation, blood was collected immediately, and kidneys were removed to determine their Mg and Ca content. Dietary fructose significantly increased kidney Ca in female rats fed deficient or adequate Mg diet and in male rats fed Mg-deficient diet only; the greatest kidney calcification occurred in female rats fed Mg-deficient diet (P less than 0.0001). Even in starch groups female rats fed the Mg-deficient diet showed some kidney Ca accumulation. The synergistic interaction of fructose and magnesium deficiency on nephrocalcinosis was significantly greater in female than in male rats. Low urinary output, optimal pH 6.8 for calcium phosphate precipitation, hypercalcaemia, hypercalciuria, hypomagnesuria, and low ratio of urinary Mg to Ca may independently or multifactorially contribute to nephrocalcinosis. The possible mechanism of this interaction is discussed.     

Nephrocalcinosis without functional renal impairment in rats subjected to subacute moderate magnesium deficiency, and intervention studies on the mobilization of calcium deposits

Female Sprague-Dawley rats (100-120 g) were kept for 12 d on diets containing 250, 1500, or 9000 ppm Mg. Then subgroups were loaded with water, frusemide or magnesium and urine was collected over 6 h. Moderately Mg-deficient diet (250 ppm) induced moderate hypomagnesaemia (62.3% of controls), but did not result in hypercalcaemia or the formation of typical erythema. Nevertheless, pronounced nephrocalcinosis developed, as shown by increased renal wet and dry weight and elevated tissue concentrations of Ca, P and Mg, the calculous deposits probably consisting to a large extent of Ca3 (PO4)2. Despite these alterations, renal function remained unimpaired in Mg-deficient rats, as shown by normal urinary creatinine excretion and the unaffected ability of the kidneys to concentrate urine. Loading with water, frusemide or Mg increased urinary excretion of calcium in all three diet groups to a similar extent; hence no significant proof can be given that calculous deposits are mobilized under these conditions. Since comparable conditions may also be present under clinical conditions in man, special care should be given to maintain optimal Mg balance.     

Decreased absorption and retention rates of magnesium in the rats fed on spinach-supplemented diets: possible explanations.

We studied the bioavailability of magnesium (Mg) in spinach after boiling with distilled water, using Mg-deficient growing male rats. The rats were fed a semipurified diet (Mg:0.063 per cent (w/w)) for 3 days. then a Mg-deficient diet (Mg:0.001 per cent (w/w)) for 5 days. They were then divided randomly into 7 groups of 6 rats each, and fed the semipurified diet (Mg: 0.063, 0.045 or 0.027 per cent (w/w)), or the spinach-supplemented diet (10 per cent (w/w) dried and powdered spinach after boiling with distilled water for 3 min at 100 degrees C). The Mg content of the diets supplemented with spinach grown on chemical nutrients, and on manure from pigs, cattle and fowl, was 0.069, 0.051, 0.043 and 0.036 per cent (w/w), respectively. Water intake and volumes of urine and faeces were significantly greater in the rats fed the spinach-supplemented diets than in those fed the semipurified diets. Apparent absorption of Mg, and urinary and faecal excretions of Mg were directly related to Mg intake: no significant difference was observed amongst the groups. Both the ratios of Mg absorption and retention were significantly lower in the rats fed diets supplemented with spinach than in those fed semipurified diets. The plasma Mg level was directly related to Mg intake in the rats fed the semipurified diets and the spinach-supplemented diets. However, the plasma Mg level in the rats fed spinach grown organically on manure from fowl tended to be higher than in the other groups. From these results, it was concluded that bound Mg in spinach was effectively utilized by Mg-deficient rats, however, the absorption and retention rates of Mg in rats fed diets supplemented with spinach were decreased. Possible explanations were discussed.     

Effect of dietary magnesium supplementation on bone loss in rats fed a high phosphorus diet.

The purpose of this study was to investigate the effect of dietary magnesium (Mg) supplementation on bone loss in rats fed a high phosphorus (P) diet. Weanling Wistar strain rats were randomly divided into four dietary groups of 6 rats each and fed their respective diets; a diet containing 0.3% P and 0.05% Mg (C), a diet containing 1.5% P and 0.05% Mg (HP), a diet containing 0.3% P and 0.15% Mg (HMg), or a diet containing 1.5% P and 0.15% Mg (HPMg), for 21 days. Compared to the C and HMg groups, serum parathyroid hormone (PTH) concentration was significantly higher in the HP and HPMg groups. Serum osteocalcin concentration and urinary excretion of C-terminal telopeptides of type I collagen (CTx), markers of bone turnover, were significantly higher in the HP and HPMg groups than in the C and HMg groups. Dietary Mg supplementation had no significant effects on serum PTH and osteocalcin concentrations, while urinary excretion of CTx was significantly lower in the HPMg group than in the HP group. These results suggested that dietary Mg supplementation suppressed bone resorption due to high P diet.     

Comparison of renal calcium concentration in obese, lean, diabetic, and non-diabetic Zucker rats fed a magnesium-deficient fructose diet.

In order to determine the effects of hypoinsulinaemia or hyperinsulinaemia on nephrocalcinosis induced by the interaction between fructose and magnesium (Mg) deficiency, we compared kidney calcification in obese versus lean, and non-diabetic versus diabetic female Zucker rats fed a magnesium-deficient fructose diet. One half of the obese and lean animals, respectively, was injected with streptozotocin to produce diabetes, and the other half was injected with citrate buffer alone. Diabetic, non-diabetic, obese, and lean animals were divided into two dietary groups, consisting of high starch or high fructose without added Mg. After a four week period, 24 hour urine was collected for urinary output, protein, oxalate, citrate, MG, and calcium (Ca) measurements. The animals were then decapitated, and blood was collected for glucose, Mg, and Ca determinations, and kidneys were removed to determine their Mg and Ca contents. All fructose-fed animals exhibited significantly more kidney Ca then the starch-fed animals. Lean non-diabetic rats fed fructose showed the greatest kidney Ca along with the greatest urinary protein excretion among all experimental groups. The significant finding in the present study is that diabetes or obesity reduced nephrocalcinosis regardless of the insulin status of the rats. Diuresis and hypercitraturia in diabetic and/or obese animals may cause a reduction in nephrocalcinosis induced by the interaction between fructose and magnesium deficiency. Hyperproteinuria (uromucoid) in combination with hypercalciuria and hypomagnesuria may be responsible for greater nephrocalcinosis in the fructose than the starch group. The possible mechanisms for this interaction on nephrocalcinosis have been discussed.     

Tissue contents and urinary excretion of taurine after administration of L-cysteine and L-2-oxothiazolidine-4-carboxylate to rats

Tissue contents and urinary excretion of taurine were studied in rats after the administration of L-cysteine and its derivatives. Average taurine content in the liver of rats fed a 25% casein diet for 7 days increased 2-fold 2h after the intraperitoneal administration of 5 mmol of L-cysteine per kg of body weight, whereas that in rats fed a 5% casein diet for 2 days increased only slightly. The difference in the liver taurine contents between these two groups was discussed in relation to cysteine dioxygenase. Taurine contents in the heart, brain and blood did not differ significantly between these two groups or between the control and the group of rats which received L-cysteine. The increase in liver taurine concentrations after L-cysteine administration was much higher than that after L-cystine administration, suggesting a difference in their absorption. The intraperitoneal administration of 5 mmol/kg of L-2-oxothiazolidine-4-carboxylate (OTCA) resulted in a 3-fold increase in liver taurine content. The average increase in taurine excretion in the 24-h urine after OTCA administration corresponded to about 6.0% and that in the next 24-h urine to about 2.6% of OTCA administered, suggesting that nearly 10% of OTCA was metabolized to taurine and excreted in the urine.     

Effect of vitamin K deficiency on urinary gamma-carboxyglutamic acid excretion in rats

Since gamma-carboxyglutamic acid (Gla) in Gla-containing proteins is stoichiometrically excreted into urine as free Gla, urinary Gla excretion is believed to reflect the rate of synthesis and degradation of vitamin K-dependent proteins and the utilization of vitamin K in body. We studied the daily changes in urinary Gla excretion and plasma vitamin K-dependent clotting factor levels in rats fed vitamin K-deficient diets followed by subcutaneous injection of vitamin K1 or after the oral administration of Warfarin. Urinary Gla excretion in normal rats fed a standard diet that contained about 500 ng of vitamin K1 per gram of diet was 2.35 +/- 0.25 mumoles/day, but the level in rats fed a markedly vitamin K-deficient diet (less than 5 ng/g) decreased to 1.40 +/- 0.14 mumoles/day. When rats were fed a moderately vitamin K-deficient diet (20-50 ng/g), plasma vitamin K-dependent clotting factor levels decreased significantly, but urinary Gla excretion did not decrease. Warfarin, a vitamin K antagonist, caused a significant decrease in urinary Gla excretion and plasma clotting factor levels. When vitamin K, (200 micrograms/kg) was injected subcutaneously in rats fed a markedly vitamin K-deficient diet, the plasma vitamin K-dependent clotting factor levels recovered quickly to normal, but urinary Gla excretion showed only a partial recovery to 1.74 +/- 0.15 mumoles/day. These results indicate that urinary Gla excretion decreases in vitamin K deficiency, but changes in urinary Gla excretion do not reflect vitamin K deficiency in rats as sensitively as changes in the prothrombin time and plasma K-dependent clotting factor levels.     

The effects of parathyroidectomy on the development of nephrocalcinosis in rats fed phosphate-supplemented and unsupplemented diets containing alpha protein.

The effects of parathyroidectomy (PTX) on the development of nephrocalcinosis in rats fed a diet containing alpha protein were investigated for the purpose of determining whether the nephrocalcinosis was phosphate-induced. PTX completely prevented the occurrence of nephrocalcinosis in rats fed a phosphate-supplemented commercial laboratory diet for 4 weeks. However, PTX did not completely prevent the occurrence of nephrocalcinosis in rats fed a phosphate-supplemented alpha protein diet. Several calciferous deposits were found in the inner medulla. The same was also found in rats that underwent sham operations and PTX rats fed the basal alpha protein diet. Total renal calcium and phosphorous levels in these three groups were also similar and were about twice as great as those in corresponding groups fed phosphate-supplemented and unsupplemented commercial laboratory diets. Therefore, we conclude that the nephrocalcinosis in rats fed a basal alpha protein diet is not induced by PTH or excess phosphate, but is induced by some other factor associated with the diet.     

Phosphate and the development of nephrocalcinosis in rats fed diets containing alpha protein.

It has been suggested that nephrocalcinosis in rats fed diets containing alkali-treated soy protein may be due to a high availability of phosphate in the diet. In the present study, the development of nephrocalcinosis in rats fed a diet containing 20% alpha protein (an alkali-treated soy protein) was compared with that in rats fed the same diet supplemented with additional phosphate. Phosphate supplementation of the alpha protein diet produced a form of nephrocalcinosis that was morphologically different, at both the light- and electronmicroscopic level, from that obtained with the unsupplemented diet but was quite similar to that obtained with a phosphate-supplemented standard commercial laboratory diet. Levels of serum and urinary calcium and phosphorus and urinary cyclic AMP suggested that a phosphate-induced secondary hyperparathyroidism was present in the rats fed either of the phosphate-supplemented diets, but not in the rats fed the unsupplemented alpha protein diet. The results of this study suggest that nephrocalcinosis in rats fed a diet containing 20% alpha protein, without additional phosphate, is not typically phosphate-induced.     

Effectiveness of a traditional Chinese medicine, Wulingsan, in suppressing the development of nephrocalcinosis induced by a high phosphorus diet in young rats

The development of nephrocalcinosis in rats fed a high phosphorus diet, and the effectiveness of the Chinese traditional medicine, Wulingsan, and its components (Poria, Alismatis Rhizoma, Atractylodis Rhizoma, Cinnamomi Ramus, Polyporus) in suppressing the development of calcinosis were studied. The rats were fed a high phosphorus diet (1.5% P) supplemented with Wulingsan or its individual components (0.5 g/kg body weight) as separate experimental groups for a 2-week period. Upon histological observation by light microscopy and electron microscopy, signs of nephrocalcinosis were observed in almost all areas of the kidney. Calculi, consisting mainly of needle-shaped crystals of hydroxyapatite, were observed in the proximal tubules, in the collecting ductal lumina, and in the mitochondria of the proximal tubular cells and the interstitial cells. X-ray microanalysis revealed that the calculi were composed of hydroxyapatite (Ca and P). In the group fed the diet supplemented with Wulingsan, the severity of calcinosis in the corticomedullary junction was only slight. In all groups fed individual components of Wulingsan, the severity of calcinosis was almost the same as that in the group fed the high phosphorus diet (1.5% P). Wulingsan suppressed the development of calcinosis in rats fed the high phosphorus diet supplemented with this Chinese medicine, whereas its individual components alone had no effect. The process of calcinosis and the mechanism responsible for the activity of this Chinese medicine in the suppression of calcinosis are discussed.     

Age decreased steady-state concentrations of genistein in plasma, liver, and skeletal muscle in Sprague-Dawley rats

Soy isoflavones are associated with low incidence of cardiovascular diseases (CVD) and hormone-dependent cancers, but no solid information is available on the relative deposition of isoflavones in the body as a function of age. One-year-old (adult) male Sprague-Dawley rats were fed control diet or one of three high-genistein isoflavone (HGI) diets at a dose of 62, 154, or 308 genistein mg/kg (ppm) diet for 5 weeks; 2-year-old (old) were fed a dose of 154 or 308 ppm. Steady-state genistein concentrations in plasma, liver, and gastrocnemius muscle of the adult rats after 12 h fast revealed a linear dose-dependent manner (P < or = 0.0001). However, there was no such relationship in the old rats. Nevertheless, old rats fed the 308 ppm genistein diet had significantly lower steady-state genistein concentrations in plasma and liver than the adult rats did (P < or = 0.05); but similar genistein concentration in muscle. The results of this study indicate that steady-state genistein concentrations in tissues of adult rats after 12 h fast exhibited a dose-dependent fashion and were diminished in specific tissues by age.     

Cholesterol-induced alteration in liver mineral concentrations in corn oil and olive oil fed rats.

This study was undertaken to compare the effects of 1% cholesterol (Ch) on some liver mineral concentrations in rats fed with corn oil (C) or olive oil (O). Male Sprague-Dawley rats (n = 4 per group) were fed AIN76A semi-purified diets containing either 5% corn oil or 5% olive oil replacing corn oil with or without 1% cholesterol for 21 days. The analysis of minerals: Phosphorous (P), Potassium (K), Magnesium (Mg), and Sulfur (S), of liver were conducted by inductively coupled plasma (ICP) spectroscopic method. In the C fed rats addition of 1% cholesterol produced significant increase in P concentrations but not K, Mg, and S concentrations. In contrast, in O fed rats, 1% Ch significantly decreased Mg and S concentrations. There was no significant change in K and P concentrations. In conclusion, this study describes the interactions between dietary oils and cholesterol on certain mineral concentrations in liver of rats. The results obtained may have clinical significance and nutritional significance in cardiovascular health.     

Moderate magnesium-restricted diet affects bone formation and bone resorption in rats.

This study investigated the effects of moderate magnesium (Mg)-restricted diet on bone formation and bone resorption in rats. Weanling Wistar strain rats were randomly divided into three dietary groups of 6 rats each and fed their respective diets; a control diet containing 0.05% Mg (C), a half Mg diet containing 0.025% Mg (1/2Mg), or a one-fifth Mg diet containing 0.01% Mg (1/5Mg), for 21 days. Serum osteocalcin level was significantly reduced with decreasing dietary Mg level. Urinary excretion of C-terminal telopeptide of type 1 collagen was significantly higher in the 1/5Mg group than in the C group. Serum insulin-like growth factor-1 (IGF-1) level was significantly lower in the 1/2Mg and 1/5Mg groups than in the C group. Serum soluble receptor activator of nuclear factor-kappaB ligand (sRANKL) level was significantly higher in the 1/2Mg and 1/5Mg groups than in the C group. These results showed that a moderate Mg-restricted diet induced a decrease in bone formation and an increase in bone resorption. Furthermore, these changes of bone formation and bone resorption might be caused by serum IGF-1 and sRANKL levels, respectively.     

Metabolism of L-cysteine in rats fed low and high protein diets

L-Cysteine (5.0 mmol per kg of body weight) was intraperitoneally injected into rats fed a 25% casein or 5% casein diet. Concentrations of acidic and neutral amino acids in various tissues were determined 2 h later. In the rats fed the 25% casein diet there was a tendency for tissue amino acid and glutathione levels to be slightly lower than controls. In the 5% casein diet group, however, concentrations of tissue amino acids and glutathione generally increased after L-cysteine administration. S-(2-Hydroxy-2-carboxyethylthio)cysteine (HCETC,3-mercaptolactate-cysteine disulfide), though in trace amounts, was detected in kidney and blood plasma in the 5% casein diet group. Increases in cysteine-glutathione disulfide in liver, kidney and erythrocytes in the 5% casein diet group were considerable. These results indicate that L-cysteine was rapidly metabolized in the 25% casein diet group through the oxidative pathway, while in the 5% casein diet group, in which liver cysteine dioxygenase activity is supposed to be quite low, the oxidative metabolism of L-cysteine decreased and part of the L-cysteine was metabolized through the transaminative pathway. Administration of 15.0 mmol L-cysteine per kg of body weight to rats fed the 25% casein diet resulted in an increase in cysteine-glutathione disulfide in liver, kidney and erythrocytes, and the appearance of HCETC in blood plasma.(ABSTRACT TRUNCATED AT 250 WORDS)     

Protective effect of severe magnesium deficiency on Plasmodium chabaudi infection

Mice were fed for 30 days on purified diets containing 50 (severely Mg deficient diet), 100 (moderately Mg deficient diet) and 1300 mg/kg (control diet). An additional group raised on stock UAR diet was also used for the experiment. The mice were maintained on the experimental diets for 12 days before being inoculated with P. chabaudi. Infection evolved similarly in mice fed the control purified diet, moderately Mg deficient diet and the stock diet whereas the severely Mg deficient diet induced a 50% decrease in malarial infection as shown by the decrease in the percentage of parasitized red blood cells (RBC). In control mice, RBC Mg values increased significantly during P. chabaudi infection; however RBC Mg values were significantly lower in Mg-deficient than in control animals.     

Magnesium-deficient diet-induced reduction in protein utilization in rats is reversed by dietary magnesium supplementation.

We investigated the effect of dietary magnesium (Mg) level on protein utilization in rats. Male Wistar rats were fed a control diet (control group) and a Mg-deficient diet (Mg-deficient group) for 28 days. After 28 days, the diet of half of the Mg-deficient group (recovery group) was changed from the Mg-deficient diet to the control diet for either 7 or 14 days. After 28 days, final body weight, weight gain and food efficiency were significantly decreased due to the Mg-deficient diet. Apparent Mg absorption, Mg retention and serum Mg levels were also significantly decreased due to the Mg-deficient diet. Furthermore, the Mg-deficient group showed a significant increase in urinary nitrogen (N) excretion and significant decreases in N retention and serum albumin level. At day 7 and 14 after changing the Mg-deficient diet to the control diet, apparent Mg absorption, Mg retention and serum Mg levels were significantly increased in the recovery group as compared with those in the Mg-deficient group. However, with regard to final body weight, weight gain and food efficiency, no significant differences were observed between the Mg-deficient group and the recovery group. At day 14 after changing the diet, urinary N excretion was significantly decreased and N retention was significantly increased in the recovery group as compared with the Mg-deficient group. At day 7 and 14 after changing the diet, the serum albumin level was also significantly increased in the recovery group as compared with that in the Mg-deficient group. These results suggest that: 1) the Mg-deficient diet depresses protein utilization; 2) the Mg-deficient diet-induced impairment of protein utilization is reversed by dietary Mg supplementation; and 3) the Mg-deficient diet-induced growth retardation is not completely reversed after 14 days of Mg supplementation.     

Diet and kidney diseases in rats

Diet-associated kidney diseases of rats includes nephropathy in both sexes and nephrocalcinosis in females. High protein content of diets appears to be the major cause for severe nephropathy and changing the source of protein to one such as soy protein, restricting caloric intake, or modifying the diet to decrease protein consumption could decrease the severity of nephropathy. The NTP-2000 diet with lower protein content than most diets decreases the severity of nephropathy and increases the survival of Fischer 344 rats without substantial changes in growth patterns and body weights. Nephrocalcinosis, characterized by mineralization of renal tubules at the corticomedullary junction, has been reported in young and adult female rats of most strains and stocks suggesting a major contribution of female sex hormones to the development of this lesion. Calcium (Ca), phosphorous (P), magnesium (Mg), and chloride (Cl) imbalances, especially a Ca:P ratio of less than 1.0 in diet, are considered to be associated with this lesion. Most commercial diets commonly used for toxicology studies have a Ca:P molar ratio of less than 1.0. Increasing the Ca:P molar ratio to more than 1.0 and closer to 1.3 in the AIN-93 purified diet and NTP-2000 nonpurified diet prevents the development of this lesion. Genetics will predispose rats to some diseases and environmental factors will influence the severity of these diseases. Diet is one of the most important environmental factors. Diets balanced for nutrients without excesses could markedly improve the health of rats used in chronic studies leading to substantial increases in survival and thereby accomplish the objective of chronic toxicity and carcinogenicity studies.     

Influence of age and hormonal treatment on intestinal absorption of magnesium in ovariectomised rats.

This study was designed to assess the effect of age, ovariectomy and estrogen treatment on the absorption and the balance of Mg in the rat. Three groups of fifteen 6- (mature), 12- (old), and 30-month-old female rats (senescent), fed a diet containing 1.5 g of Mg/kg were used in the present study. Within each group, 10 rats were surgically ovariectomized (OVX). From day 2 until day 60 after OVX, they were s.c. injected with either solvant or 17 beta-estradiol (E: 10 mg/kg bw/48 h, n = 5). Five other rats were sham operated (SH, n = 5) and received solvent alone. Animals were pair fed 6 g/100 g bw/day and distilled water was available ad libitum. Food intake, urine and feces from each individual rat were measured 1 day per week, during the last 5 weeks. The results clearly showed that apparent Mg absorption (per cent) was not significantly altered with aging. Moreover, whatever the age, neither OVX nor E treatment had any significant effect on Mg apparent absorption.     

不同脂肪含量的高脂纯化配方饲料对大、小鼠代谢综合征发生的影响

 摘要： 目的 探讨不同脂肪含量的高脂纯化配方饲料对大、小鼠体重、血糖、血胰岛素、血脂、脂肪肝及白蛋白尿的影响。 方法 雄性SD大鼠及C57BL/6小鼠随机分为MS10%、MS45%和MS60%脂肪含量饲料组,喂养3个月,检测动物体重、血糖、血胰岛素水平、血脂和蛋白尿水平,以及主要脏器重量及肝脏脂质含量。 结果 与正常组（MS10%脂肪含量）相比,高脂组（MS45%和MS60%脂肪含量）动物体重显著增加,出现明显的糖耐量异常、胰岛素抵抗和血脂水平升高,同时伴有肝脏脂质含量和蛋白尿水平的增加,并且以MS45%高脂组体重增加及胰岛素抵抗更加显著。 结论 MS45%和MS60%高脂配方饲料均可在大、小鼠较好地诱导代谢综合征的发生,而且前者优于后者。 关键词： 高脂饲料;胰岛素抵抗;肥胖;代谢综合征