Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0948265 (
metabolic syndrome
)
24,271
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Individuals with
metabolic syndrome
(MetS) often have elevated plasma plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (t-PA), contributing to an increased risk of cardiovascular disease. PAI-1 and t-PA may be affected by chronic (n-3) long-chain PUFA [(n-3)LCPUFA] supplementation; however, the acute impact of fat ingestion on these risk factors has not been established. Our objective was to investigate the acute effect of (n-3)LCPUFA on plasma PAI-1, t-PA, and platelet aggregation. We conducted a randomized crossover study in which men (n = 8, > or =45 y) with MetS consumed
water
or a high-saturated fat beverage (1 g fat/kg body weight) with either a high or low content of (n-3)LCPUFA. Blood samples were collected over 8 h to measure triacylglycerol (TAG), PAI-1, t-PA, and platelet aggregation. Both fat loads resulted in a significant increase in whole blood TAG concentration, plasma PAI-1 and t-PA concentrations, and PAI-1 activity, as well as a significant decrease in t-PA activity during the postprandial period. Interestingly, PAI-1 concentration and activity increased more following the high (n-3)LCPUFA compared with the low (n-3)LCPUFA beverage (P < 0.05). Furthermore, the high (n-3)LCPUFA beverage resulted in a lower t-PA activity (P < 0.05), whereas the effects of the 2 fat loads on the plasma t-PA concentration and platelet aggregation did not differ. Overall, acute intake of a high (n-3)LCPUFA beverage shifted the balance between plasma PAI-1 and t-PA, which might indicate a lower capacity for fibrinolysis.
...
PMID:Acute ingestion of long-chain (n-3) polyunsaturated fatty acids decreases fibrinolysis in men with metabolic syndrome. 1988 9
The mechanisms of how tea and epigallocatechin-3-gallate (EGCG) lower body fat are not completely understood. This study investigated long-term administration of green tea (GT), black tea (BT), or isolated EGCG (1 mg/kg per day) on body composition, glucose tolerance, and gene expression related to energy metabolism and lipid homeostasis; it was hypothesized that all treatments would improve the indicators of
metabolic syndrome
. Rats were fed a 15% fat diet for 6 months from 4 weeks of age and were supplied GT, BT, EGCG, or
water
. GT and BT reduced body fat, whereas GT and EGCG increased lean mass. At 16 weeks GT, BT, and EGCG improved glucose tolerance. In the liver, GT and BT increased the expression of genes involved in fatty acid synthesis (SREBP-1c, FAS, MCD, ACC) and oxidation (PPAR-alpha, CPT-1, ACO); however, EGCG had no effect. In perirenal fat, genes that mediate adipocyte differentiation were suppressed by GT (Pref-1, C/EBP-beta, and PPAR-gamma) and BT (C/EBP-beta), while decreasing LPL, HSL, and UCP-2 expression; EGCG increased expression of UCP-2 and PPAR-gamma genes. Liver triacylglycerol content was unchanged. The results suggest that GT and BT suppressed adipocyte differentiation and fatty acid uptake into adipose tissue, while increasing fat synthesis and oxidation by the liver, without inducing hepatic fat accumulation. In contrast, EGCG increased markers of thermogenesis and differentiation in adipose tissue, while having no effect on liver or muscle tissues at this dose. These results show novel and separate mechanisms by which tea and EGCG may improve glucose tolerance and support a role for these compounds in obesity prevention.
...
PMID:Green tea, black tea, and epigallocatechin modify body composition, improve glucose tolerance, and differentially alter metabolic gene expression in rats fed a high-fat diet. 1993 67
The article critically reviews selected, clinically significant, adverse endocrine and metabolic effects associated with psychotropic drug treatments, including hyperprolactinaemia, hyponatraemia, diabetes insipidus, hypothyroidism, hyperparathyroidism, sexual dysfunction and virilization, weight loss, weight gain and
metabolic syndrome
(type 2 diabetes mellitus, dyslipidaemia and hypertension). Such effects are prevalent and complex, but can be managed clinically when recognized. They encourage continued critical assessment of benefits versus risks of psychotropic drugs and underscore the importance of close coordination of psychiatric and general medical care to improve long-term health of psychiatric patients. Options for management of hyperprolactinaemia include lowering doses, switching to agents such as aripiprazole, clozapine or quetiapine, managing associated osteoporosis, carefully considering the use of dopamine receptor agonists and ruling out stress, oral contraceptive use and hypothyroidism as contributing factors. Disorders of
water
homeostasis may include syndrome of inappropriate antidiuretic hormone (SIADH), managed by
water
restriction or slow replacement by hypertonic saline along with drug discontinuation. Safe management of diabetes insipidus, commonly associated with lithium, involves switching mood stabilizer and consideration of potassium-sparing diuretics. Clinical hypothyroidism may be a more useful marker than absolute cut-offs of hormone values, and may be associated with quetiapine, antidepressant and lithium use, and managed by thyroxine replacement. Hyper-parathyroidism requires comprehensive medical evaluation for occult tumours. Hypocalcaemia, along with multiple other psychiatric and medical causes, may result in decreased bone density and require evaluation and management. Strategies for reducing sexual dysfunction with psychotropics remain largely unsatisfactory. Finally, management strategies for obesity and
metabolic syndrome
are reviewed in light of the recent expert guidelines, including risk assessment and treatments, such as monoamine transport inhibitors, anticonvulsants and cannabinoid receptor antagonists, as well as lifestyle changes.
...
PMID:Adverse endocrine and metabolic effects of psychotropic drugs: selective clinical review. 1995 39
Benzylamine is found in Moringa oleifera, a plant used to treat diabetes in traditional medicine. In mammals, benzylamine is metabolized by semicarbazide-sensitive amine oxidase (SSAO) to benzaldehyde and hydrogen peroxide. This latter product has insulin-mimicking action, and is involved in the effects of benzylamine on human adipocytes: stimulation of glucose transport and inhibition of lipolysis. This study examined whether chronic, oral administration of benzylamine could improve glucose tolerance and the circulating lipid profile without increasing oxidative stress in overweight and pre-diabetic mice. The benzylamine diffusion across the intestine was verified using everted gut sacs. Then, glucose handling and metabolic markers were measured in mice rendered insulin-resistant when fed a high-fat diet (HFD) and receiving or not benzylamine in their drinking
water
(3600micromol/(kgday)) for 17 weeks. HFD-benzylamine mice showed lower body weight gain, fasting blood glucose, total plasma cholesterol and hyperglycaemic response to glucose load when compared to HFD control. In adipocytes, insulin-induced activation of glucose transport and inhibition of lipolysis remained unchanged. In aorta, benzylamine treatment partially restored the nitrite levels that were reduced by HFD. In liver, lipid peroxidation markers were reduced. Resistin and uric acid, surrogate plasma markers of
metabolic syndrome
, were decreased. In spite of the putative deleterious nature of the hydrogen peroxide generated during amine oxidation, and in agreement with its in vitro insulin-like actions found on adipocytes, the SSAO-substrate benzylamine could be considered as a potential oral agent to treat
metabolic syndrome
.
...
PMID:Chronic benzylamine administration in the drinking water improves glucose tolerance, reduces body weight gain and circulating cholesterol in high-fat diet-fed mice. 2004 61
To establish animal models with diet-induced metabolic disorders similar to human
metabolic syndrome
, 2 unhealthy dietary habits featuring a high fat content and a sucrose-containing beverage intake, alone or in combination, were tested on Wistar rats and C57BL/6J mice. The 2 dietary habits were, respectively, simulated by feeding a high-fat diet (regimen A) or additionally providing 30% sucrose (wt/vol) in the drinking
water
(regimen B). Using a 2 x 2 factorial design, 4 groups of animals were fed chow diet plus plain
water
(group C), high-fat diet (30% [wt/wt] fat) plus plain
water
(group A), chow diet plus sucrose in drinking
water
(group B), and high-fat diet plus sucrose in drinking
water
(group AB) for 26 weeks. In Wistar rats, regimen B caused a significant increase in visceral fat; serum levels of lipids, glucose, insulin, and uric acid; insulin resistance; and blood pressure, whereas regimen A only caused a significant increase in visceral fat and serum insulin levels (P < .05). In contrast, regimen A induced a full array of
metabolic syndrome
in C57BL/6J mice; but regimen B only caused slight obesity and hyperlipidemia. In both Wistar rats and C57BL/6J mice, there were no additive effects of the 2 regimens, indicated by significant interactions between regimens A and B on the metabolic indexes measured. These results show that, in terms of inducing
metabolic syndrome
, Wistar rats are more responsive to sucrose
water
regimen, whereas C57BL/6J mice are more responsive to the high-fat diet regimen.
...
PMID:Two unhealthy dietary habits featuring a high fat content and a sucrose-containing beverage intake, alone or in combination, on inducing metabolic syndrome in Wistar rats and C57BL/6J mice. 2004 37
In this study, we investigated the effects of the branched-chain amino acid l-isoleucine (Ile) on both obesity and glucose/fat homeostasis in mice that were fed a high-fat (45% energy) diet. The mice were divided into different treatment groups and given a high-fat diet for 6 wk. During the last 4 wk, Ile was dissolved and added to the drinking
water
to a final concentration of 2.5%. The control mice received vehicle alone. The mice in the Ile group had an almost 6% lower body weight gain and 49% less epididymal white adipose tissue (WAT) mass with the control group (P < 0.05). The hepatic and skeletal muscle triglyceride (TG) concentrations and degree of hyperinsulinemia in the Ile group mice were also lower than the control group by 38, 47, and 39%, respectively (P < 0.05). The WAT leptin concentration was also lower, whereas that of adiponectin was higher, in the Ile group compared with the control group (P < 0.05). The hepatic levels of protein CD36/fatty acid translocase, PPARalpha, and uncoupling protein (UCP) 2 and the levels of UCP3 in skeletal muscle were all greater in the Ile group than in the control mice (P < 0.05). These results demonstrate that the liver and muscle TG concentrations are both lowered by Ile treatment. In addition, the PPARalpha and UCP expression levels in the mouse tissues were greater in the Ile group compared with the controls. Our current data thus suggest that supplementation with Ile might be useful in the treatment of
metabolic syndrome
.
...
PMID:Isoleucine prevents the accumulation of tissue triglycerides and upregulates the expression of PPARalpha and uncoupling protein in diet-induced obese mice. 2008 73
We have demonstrated previously that both acute and chronic oral administration of adenosine have novel functions such as anti-hypertensive effects and improved hyperlipidaemia in stroke-prone spontaneously hypertensive rats (SHRSP) fed a normal diet. The purpose of the present study was to investigate the effect of adenosine administration on
metabolic syndrome
-related parameters in SHRSP fed a high-fat diet. Six-week-old rats were divided into three groups, and were administered either
water
(control) or adenosine (10 or 100 mg/l) for 8 weeks. During this period, the rats had free access to a high-fat diet based on AIN-93M. The results showed that hypertension, plasma lipid, NO, insulin, glucose and urinary 8-hydroxy-2'-deoxyguanosine levels improved significantly in both adenosine groups. The mRNA expression levels of genes involved in anti-oxidative activity and adenosine receptors were also altered in the adenosine groups. Administration of adenosine also increased plasma adiponectin levels, accompanied by upregulation of mRNA expression level of adiponectin and adiponectin receptor 1 in perirenal fat and adiponectin receptor 2 in the liver. In conclusion, oral administration of adenosine is effective for improving
metabolic syndrome
-related parameters in SHRSP, and accordingly it may prevent the progression of the
metabolic syndrome
.
...
PMID:Anti-metabolic syndrome effects of adenosine ingestion in stroke-prone spontaneously hypertensive rats fed a high-fat diet. 2017 42
Pioglitazone is prescribed to improve insulin sensitivity in type 2 diabetes mellitus patients and has been discussed as a therapy for
metabolic syndrome
. Pioglitazone and other thiazolidinediones are associated with fluid retention and edema that may exacerbate existing or developing congestive heart failure, which is often present in these patients. Using a nonhuman primate model, our aims were to evaluate (1) whether fluid shifts were detectable in normoglycemic monkeys, (2) which fluid compartment changed, and (3) whether fluid retention was dose dependent. Seventeen adult male cynomolgus macaques (Macaca fascicularis) were studied in a Latin square design such that all animals received 0, 1, 2, and 5 mg/kg pioglitazone for 6 weeks with 2 weeks of washout between dosing intervals. Doses approximated human exposures achieved with 30, 45, and 60 mg. At the end of each period, animals were weighed and underwent dual-absorption x-ray absorption scanning for body composition measurements. Fluid volumes were quantitated by Evans blue dilution for plasma volume, equilibration of sodium bromide for extracellular
water
, and deuterated
water
for total body
water
. Significant (P < .05) effects were seen with expansion of PV at both the 2- and 5-mg/kg doses, along with reduced plasma sodium at 5 mg/kg; however, surrogate end points used to indicate fluid retention (body weight, hematocrit, total protein, and albumin) did not change significantly. Significant trends toward increases in interstitial fluid and extracellular
water
with increasing dose were apparent. Pioglitazone effectively improved metabolic status by significantly decreasing fasting glucose and triglycerides and increasing adiponectin. We conclude that thiazolidinedione-related plasma volume expansion occurs in nondiabetic primates and that fluid retention is detectable when compartments are directly measured.
...
PMID:Fluid compartmental shifts with efficacious pioglitazone therapy in overweight monkeys: implications for peroxisome proliferator-activated receptor-gamma agonist use in prediabetes. 2019 97
Numerous clinical and experimental studies have linked stress to changes in risk factors associated with the development of physiological syndromes, including metabolic disorders. How different mediators of the stress response, such as corticosterone (CORT), influence these changes in risk remains unclear. Although CORT has beneficial short-term effects, long-term CORT exposure can result in damage to the physiological systems it protects acutely. Disruption of this important physiologic signal is observed in numerous disparate disorders, ranging from depression to Cushing's syndrome. Thus, understanding the effects of chronic high CORT on metabolism and physiology is of key importance. We explored the effects of 4-wk exposure to CORT dissolved in the drinking
water
on the physiology and behavior of male mice. We used this approach as a noninvasive way of altering plasma CORT levels while retaining some integrity in the diurnal rhythm present in normal animals. This approach has advantages over methods involving constant CORT pellets, CORT injections, or adrenalectomy. We found that high doses of CORT (100 microg/ml) result in rapid and dramatic increases in weight gain, increased adiposity, elevated plasma leptin, insulin and triglyceride levels, hyperphagia, and decreased home-cage locomotion. A lower dose of CORT (25 microg/ml) resulted in an intermediate phenotype in some of these measures but had no effect on others. We propose that the physiological changes observed in the high-CORT animals approximate changes observed in individuals suffering from the
metabolic syndrome
, and that they potentially serve as a model for hypercortisolemia and stress-related obesity.
...
PMID:Endocrine and physiological changes in response to chronic corticosterone: a potential model of the metabolic syndrome in mouse. 2021 72
Recent evidence suggests that treatment with mineralocorticoid receptor antagonist suppressed local inflammation in vascular tissues or cardiomyocytes; therefore, we examined the effect of spironolactone on glucose and lipid metabolism in a mouse model with diet-induced diabetes and nonalcoholic fatty liver disease. C57BL/6 mice were fed either the control diet, 60% fat diet with 30% fructose
water
(HFFD), or HFFD with spironolactone for 8 wk. HFFD mice demonstrated apparent phenotypes of
metabolic syndrome
, including insulin resistance, hypertension, dyslipidemia, and fatty liver. Although treatment with spironolactone did not affect the increased calorie intake and body weight by HFFD, the increments of epididymal fat weight, blood pressure, serum triglyceride, free fatty acids, leptin, and total cholesterol levels were significantly suppressed. Elevation of blood glucose during glucose and insulin tolerance tests in HFFD mice was significantly lowered by spironolactone. Notably, increased glucose levels during pyruvate tolerance test in HFFD mice were almost completely ameliorated to control levels by the treatment. Staining with hematoxylin-eosin (HE) and Oil-red-O demonstrated marked accumulation of triglycerides in the centrilobular part of the hepatic lobule in HFFD mice, and these accumulations were effectively improved by spironolactone. Concomitantly HFFD feeding markedly up-regulated hepatic mRNA expression of proinflammatory cytokines (TNFalpha, IL-6, and monocyte chemoattractant protein-1), gluconeogenic gene phosphoenolpyruvate carboxykinase, transcription factor carbohydrate response element binding protein, and its downstream lipogenic enzymes, all of which were significantly suppressed by spironolactone. These results indicate that inhibition of mineralocorticoid receptor might be a beneficial therapeutic approach for diet-induced phenotypes of
metabolic syndrome
and fatty liver.
...
PMID:Spironolactone improves glucose and lipid metabolism by ameliorating hepatic steatosis and inflammation and suppressing enhanced gluconeogenesis induced by high-fat and high-fructose diet. 2021 73
<< Previous
1
2
3
4
5
6
7
8
9
10
Next >>