Role of n-3 Polyunsaturated Fatty Acids in Ameliorating the Obesity-Induced Metabolic Syndrome in Animal Models and Humans

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glucose intolerance 1 endocrinologydiseases
hyperglycemia 1 endocrinologydiseases
hyperlipidemia 1 endocrinologydiseases
metabolic syndrome 30 endocrinologydiseases
obesity 50 endocrinologydiseases
alpha-linolenic acid 1 endocrinologydiseasesdrugs
childhood obesity 3 endocrinologydiseases

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alpha-linolenic acid 5648 recommendations for n-3 PUFA intake because of their beneficial effects [[18]]. In humans, the conversion from alpha-linolenic acid (ALA; C18:3 n-3) to EPA is low (~8%) with even lower conversion to DHA (<0.1%) [[19],[20]]. In rodents
Select Disease Character Offset Disease Term Instance
childhood obesity 19079 worldwide [[81]], and the modulation of fat intake and its composition in the early-life period may prevent childhood obesity [[82]]. A large cohort study shows increased fat cell numbers and size starting from age three [[83]].
childhood obesity 19271 starting from age three [[83]]. Modulation of fat intake and its composition in early life may prevent childhood obesity [[82]]. Higher n-3 PUFA concentrations in the maternal diet and in the umbilical cord plasma phospholipids
childhood obesity 19994 lipid esterification pathways and reduces placental lipid accumulation [[84]]. Hence, reduced risk of childhood obesity is associated with enhanced maternal-fetal-neonatal n-3 PUFA.A number of systematic reviews indicate
glucose intolerance 43915 and translocation of GLUT4 to the plasma membrane [[99]]. Mice deficient in GPR120 develop obesity, glucose intolerance and fatty livers, suggesting that GPR120 plays a role in lipid metabolism.6.3. Energy ExpenditureLong-chain
hyperglycemia 2426 both immune and non-immune cells [[2]]. Consequently, obesity and its comorbidities, characterized by hyperglycemia , dyslipidemia, abdominal obesity, low-grade systemic inflammation, hypertension, elevated plasma triacylglycerol
hyperlipidemia 21353 especially DHA, can lower plasma TAG in healthy subjects. Moreover, n-3 PUFA not only improves the hyperlipidemia in healthy populations, but also ameliorates dyslipidemia in overweight and obese individuals [[75]].
metabolic syndrome 2601 inflammation, hypertension, elevated plasma triacylglycerol (TAG) and cholesterol, may lead to the onset of metabolic syndrome , a serious threat to the health of the population [[1],[3]]. The major cause of obesity is the chronic
metabolic syndrome 6323 phospholipids. n-3 PUFA are not only essential nutrients, but also beneficial mediators for preventing metabolic syndrome .However, perhaps the best remedy for obesity, metabolic syndrome or non-alcoholic fatty liver disease
metabolic syndrome 6388 beneficial mediators for preventing metabolic syndrome.However, perhaps the best remedy for obesity, metabolic syndrome or non-alcoholic fatty liver disease prevention is caloric restriction and/or increased energy expenditure.
metabolic syndrome 6565 restriction and/or increased energy expenditure. TAG is a marker for total fats in circulation and metabolic syndrome , which is associated with increased plasma TAG [[24]]. Thus, to lower the plasma TAG oxidation or storage
metabolic syndrome 8326 inflammation. The review will also address the specific effects of n-3 PUFA to ameliorate obesity-induced metabolic syndrome (Figure 1). Although this review is focused on the effects and metabolism of n-3 PUFA in adipose tissue,
metabolic syndrome 9568 of WAT and BAT lipid metabolism could yield strategies to prevent and manage obesity and the related metabolic syndrome .WAT is a highly plastic and dynamic tissue and accounts for less than 5% of body weight in very lean
metabolic syndrome 15509 (Figure 2) [[58]]. Elevated ALA concentration in adipose tissues is associated with lower prevalence of metabolic syndrome , and D6D may affect the conversion of ALA to EPA [[59]].Resolvins and protectins are newly-discovered
metabolic syndrome 16682 concentrations in plasma than in erythrocytes [[66]], and the plasma n-3 PUFA are negatively correlated with metabolic syndrome [[67],[68]]. Conversely, higher plasma levels of n-3 PUFA are associated with reduced obesity risk [[69]].
metabolic syndrome 17058 circulation via dietary supplementation to reduce plasma TAG can lower the incidence of the obesity-induced metabolic syndrome , including insulin resistance, hypertension and dyslipidemia. Moreover, dietary PUFA supplementation
metabolic syndrome 17630 status may influence the fetus or the neonate to modulate the incidence of obesity and obesity-induced metabolic syndrome later in life; Secondly, dietary n-3 PUFA has been shown to be beneficial in children, as well, suggesting
metabolic syndrome 17993 improves health outcomes and decreases obesity risk in adults, reducing the risk of obesity-related metabolic syndrome . The results of selected human trials regarding n-3 effects are summarized in Table 1.5.1.1. The Effects
metabolic syndrome 21673 systemic inflammation [[88]]. The intake of 0.3–3.0 g n-3 PUFA/day reduces body weight, body fats and metabolic syndrome in overweight, obese individuals and metabolic syndrome [[30],[76]]. Replacement of neutral fats in
metabolic syndrome 21729 PUFA/day reduces body weight, body fats and metabolic syndrome in overweight, obese individuals and metabolic syndrome [[30],[76]]. Replacement of neutral fats in the diet with fish oils reduces body fat mass (fish oil
metabolic syndrome 21958 control = −0.88 ± 0.16 vs. −0.3 ± 0.34 kg) [[89]]. Thus, n-3 PUFA attenuates the characteristics of metabolic syndrome , such as lowering of plasma TAG and body fat mass.5.1.2. The Effects of n-3 PUFA on Inflammation Factors
metabolic syndrome 22936 adults.In men, during a four-year follow-up period, n-3 PUFA intake is inversely associated with risk for metabolic syndrome , and high n-3 PUFA consumption significantly lowers the risk. On the other hand, there is no association
metabolic syndrome 23085 significantly lowers the risk. On the other hand, there is no association between the incidence of metabolic syndrome and the intake of fish and n-3 PUFA in women [[93]]. The result shows the potential sex difference in
metabolic syndrome 23336 PUFA supplementation. A combination of weight loss and n-3 PUFA supplementation reduces markers of metabolic syndrome without affecting the levels of inflammatory markers [[77],[78]]. In moderately obese men, MCP-1, but
metabolic syndrome 24884 HDHA), is increased [[96]]. The biologically-active SPM may contribute to the benefits of n-3 PUFA in metabolic syndrome . In contrast, in patients with elevated TAG levels supplemented with n-3 PUFA for 10 weeks, no RvE1,
metabolic syndrome 25245 diabetes may limit the beneficial effect of n-3 fatty acids in reversing the deleterious effect of metabolic syndrome . However, larger scale population and mechanistic studies may be required to uncover the beneficial
metabolic syndrome 27315 correlate positively with the degree of fatty livers, but only omental adipocyte size is related to metabolic syndrome [[104]]. Moreover, variation in a rate-limiting gene for PUFA synthesis, Δ 6-desaturase, can affect
metabolic syndrome 27453 variation in a rate-limiting gene for PUFA synthesis, Δ 6-desaturase, can affect the prevalence of metabolic syndrome [[59]]. The lack of a consistent study design and variations in human responsiveness may be major limitations
metabolic syndrome 30314 a beneficial role in reducing adiposity and therefore to lower the incidence of the obesity-induced metabolic syndrome [[112]]. For example, in rats fed a diet with a high concentration of either saturated fatty acids (coconut
metabolic syndrome 32991 diets may reduce beneficial SPM generated from n-3 PUFA and increase the incidence of obesity-induced metabolic syndrome . Taken together, n-3 PUFA reduce plasma TAG, suppress adipose tissue inflammation and enhance adipose
metabolic syndrome 35324 insulin sensitivity is enhanced [[130]].Most rodent studies feed a high-energy diet and try to ameliorate metabolic syndrome symptoms with supplements of n-3 PUFA. However, diets containing n-3 PUFA in rodent studies tend to
metabolic syndrome 47024 observations suggest that obesity may impair TRPV1 functions or expression, and DHA may prevent obesity and metabolic syndrome partly through restoring TRPV1 function.In addition to the ion channel receptor TRPV1 and GPR120, another
metabolic syndrome 57149 individual source is highly variable [[24],[199]]. The plasma lipid profile plays an important role in metabolic syndrome incidence and severity [[67],[68],[200]]. Techniques for high-throughput and sensitive analysis of blood
metabolic syndrome 58596 PPARδ [[205]], suggesting that not only a GPR120 agonist, but a D6D inducer may lower the prevalence of metabolic syndrome . However, a gender difference must be considered because estrogen increases the D5D and D6D activity
metabolic syndrome 58765 because estrogen increases the D5D and D6D activity [[206]].The goal of ameliorating the symptoms of metabolic syndrome to a large extent involves lowering ectopic fat deposition by decreasing hepatic lipogenesis/adipogenesis
metabolic syndrome 59043 interplay between adipose and liver tissues influenced by n-3 PUFA is an important contributor to control metabolic syndrome . However, n-3 PUFA also regulate lipid and glucose metabolism in muscles and pancreatic islets by preventing
metabolic syndrome 59240 pancreatic islets by preventing lipotoxicity and inflammation [[207],[208]]. An effective control of metabolic syndrome will require a comprehensive understanding of lipid and carbohydrate metabolism not only in adipose
obesity 800 kajuwon@purdue.eduPublication date (epub): 10/2016Publication date (collection): 10/2016AbstractThe incidence of obesity and its comorbidities, such as insulin resistance and type II diabetes, are increasing dramatically,
obesity 1154 the body. An excess of adipose mass accumulation caused by chronic positive energy balance results in obesity . The n-3 polyunsaturated fatty acids (n-3 PUFA), DHA (docosahexaenoic acid) and EPA (eicosapentaenoic
obesity 2161 expression are highlighted. The beneficial effects of n-3 PUFA may help to reduce the incidence of obesity and its comorbidities.1. IntroductionObesity has become a health problem worldwide [[1]], and it leads
obesity 2378 increase activation of inflammatory signaling in both immune and non-immune cells [[2]]. Consequently, obesity and its comorbidities, characterized by hyperglycemia, dyslipidemia, abdominal obesity, low-grade systemic
obesity 2465 Consequently, obesity and its comorbidities, characterized by hyperglycemia, dyslipidemia, abdominal obesity , low-grade systemic inflammation, hypertension, elevated plasma triacylglycerol (TAG) and cholesterol,
obesity 2700 metabolic syndrome, a serious threat to the health of the population [[1],[3]]. The major cause of obesity is the chronic excessive energy intake from calorie-dense foods, such as high fat foods that contain
obesity 6379 but also beneficial mediators for preventing metabolic syndrome.However, perhaps the best remedy for obesity , metabolic syndrome or non-alcoholic fatty liver disease prevention is caloric restriction and/or increased
obesity 8310 expenditure and inflammation. The review will also address the specific effects of n-3 PUFA to ameliorate obesity -induced metabolic syndrome (Figure 1). Although this review is focused on the effects and metabolism
obesity 9023 nutrition, metabolism and molecular mechanisms. Keywords used in each electronic database search included obesity , diabetes, adipose tissue, fatty acids, fish oil, n-3 polyunsaturated fatty acid (n-3 PUFA), animal
obesity 9544 Knowledge regarding regulation of WAT and BAT lipid metabolism could yield strategies to prevent and manage obesity and the related metabolic syndrome.WAT is a highly plastic and dynamic tissue and accounts for less
obesity 10047 and degradation of TAG and fatty acid oxidation in adipocytes. Excessive accumulation of WAT leads to obesity , which may be caused by an increase in adipocyte numbers (hyperplasia) and/or adipocyte size (hypertrophy)
obesity 10303 consequence of increased fat mass rather than a factor preceding the development of being overweight/ obesity because increased lipolysis during the development of obesity would be expected to decrease fat mass.
obesity 10365 preceding the development of being overweight/obesity because increased lipolysis during the development of obesity would be expected to decrease fat mass. Adipose tissue mass is also determined by the rate of lipid
obesity 11035 ~25% in obese people with insulin resistance [[36]]. The reduction in adipogenic gene expression with obesity suggests that adipocytes from obese mice or humans have a plateaued lipogenic capacity, leading to a
obesity 16495 n-3 PUFAThe type and quantity of fats in the diet are important factors in determining the risk for obesity [[65]]. The correlation of dietary fatty acid intake is stronger with concentrations in plasma than
obesity 16787 metabolic syndrome [[67],[68]]. Conversely, higher plasma levels of n-3 PUFA are associated with reduced obesity risk [[69]]. ALA conversion to longer chain n-3 PUFA, such as EPA and possibly DHA, may provide cardioprotection
obesity 17042 in the circulation via dietary supplementation to reduce plasma TAG can lower the incidence of the obesity -induced metabolic syndrome, including insulin resistance, hypertension and dyslipidemia. Moreover, dietary
obesity 17602 that maternal nutritional status may influence the fetus or the neonate to modulate the incidence of obesity and obesity-induced metabolic syndrome later in life; Secondly, dietary n-3 PUFA has been shown to be
obesity 17614 nutritional status may influence the fetus or the neonate to modulate the incidence of obesity and obesity -induced metabolic syndrome later in life; Secondly, dietary n-3 PUFA has been shown to be beneficial
obesity 17932 the early postnatal years; Lastly, n-3 PUFA supplementation improves health outcomes and decreases obesity risk in adults, reducing the risk of obesity-related metabolic syndrome. The results of selected human
obesity 17977 supplementation improves health outcomes and decreases obesity risk in adults, reducing the risk of obesity -related metabolic syndrome. The results of selected human trials regarding n-3 effects are summarized
obesity 18893 and adipokine gene expression in adipose tissues, which may potentially lead to the development of obesity later in life [[80]]. Obesity in children is increasing in prevalence worldwide [[81]], and the modulation
obesity 19089 and the modulation of fat intake and its composition in the early-life period may prevent childhood obesity [[82]]. A large cohort study shows increased fat cell numbers and size starting from age three [[83]].
obesity 19281 age three [[83]]. Modulation of fat intake and its composition in early life may prevent childhood obesity [[82]]. Higher n-3 PUFA concentrations in the maternal diet and in the umbilical cord plasma phospholipids
obesity 20004 esterification pathways and reduces placental lipid accumulation [[84]]. Hence, reduced risk of childhood obesity is associated with enhanced maternal-fetal-neonatal n-3 PUFA.A number of systematic reviews indicate
obesity 21529 overweight and obese individuals [[75]]. High EPA and DHA intakes also attenuate the association of obesity with dyslipidemia and low-grade systemic inflammation [[88]]. The intake of 0.3–3.0 g n-3 PUFA/day
obesity 25135 detected [[97]]. These divergent findings suggest that insufficient SPM biosynthesis from n-3 PUFA in obesity or diabetes may limit the beneficial effect of n-3 fatty acids in reversing the deleterious effect of
obesity 25954 may attenuate beneficial n-3 PUFA effects and the secretion of glucagon-like peptide 1, leading to obesity [[101]]. Furthermore, the expression of the fatty acid binding protein 4 in omental adipose tissue is
obesity 26840 conditions, general daily diet quality and quantity, etc. Another potential confounding factor, benign obesity , defined as metabolically healthy obese individuals (MHO) that are insulin sensitive with lower levels
obesity 28979 increased in high-fat-fed fat-1 mice. These results indicate that restoration of n-3 PUFA prevents obesity -linked inflammation and insulin resistance [[106]]. Thus, endogenous n-3 PUFA is beneficial for coping
obesity 30298 n-3 PUFAs play a beneficial role in reducing adiposity and therefore to lower the incidence of the obesity -induced metabolic syndrome [[112]]. For example, in rats fed a diet with a high concentration of either
obesity 32591 tissue function and protect the liver from insulin resistance and hepatic steatosis in murine models of obesity [[120]]. Defective SPM biosynthesis from n-3 PUFA caused by adipose tissue inflammation [[121]] can
obesity 32975 ratio in modern diets may reduce beneficial SPM generated from n-3 PUFA and increase the incidence of obesity -induced metabolic syndrome. Taken together, n-3 PUFA reduce plasma TAG, suppress adipose tissue inflammation
obesity 37800 Understanding the processes that lead to de novo differentiation of adipocytes and the progression to obesity is necessary [[119]]. Individual n-3 PUFA may function as agonists or antagonists for several transcription
obesity 41311 fully-differentiated 3T3-L1 cells after a four-hour incubation. The results suggest that DHA may exert is anti- obesity effect by inducing apoptosis in post-confluent preadipocytes [[147]]. To compare results in these in
obesity 43906 transport and translocation of GLUT4 to the plasma membrane [[99]]. Mice deficient in GPR120 develop obesity , glucose intolerance and fatty livers, suggesting that GPR120 plays a role in lipid metabolism.6.3.
obesity 46825 tissues, indicating the expression of TRPV1 in adipocytes may play a role in preventing adipogenesis and obesity . Obese human male subjects have reduced TRPV1 expression [[160]]. Therefore, these observations suggest
obesity 46942 human male subjects have reduced TRPV1 expression [[160]]. Therefore, these observations suggest that obesity may impair TRPV1 functions or expression, and DHA may prevent obesity and metabolic syndrome partly
obesity 47012 these observations suggest that obesity may impair TRPV1 functions or expression, and DHA may prevent obesity and metabolic syndrome partly through restoring TRPV1 function.In addition to the ion channel receptor
obesity 48276 though adipocytes were initially thought to be the cellular source of proinflammatory mediators in obesity , it was later established that infiltrated macrophages in obese fat are the major source of exacerbated
obesity 53012 major apolipoprotein of high density lipoprotein [[165]]. Serum SAA is correlated with the degree of obesity [[183]]. Human recombinant SAA inhibits the expression of lipogenesis-related genes and promotes the
obesity 54099 effects mediated by DHA to alter lipid metabolism could be a new approach to cope with the incidence of obesity .7.2.2. Fibroblast Growth Factor 21Physiologically, liver, but not adipose tissue, is the major source
obesity 57426 Thus, routine plasma examination could be applied for monitoring health status.To treat patients with obesity or its comorbidities, the amount of fish oils required to appropriately serve as ligands for the n-3
obesity 57761 Although n-3 PUFA also play a role as PPAR ligands, a synthetic PPARγ agonist reduces the symptoms of obesity , but also has many side effects, including induction of weight gain, fluid retention and bone fractures
obesity 58121 administration of n-3 PUFA-derived SPM mediators may resolve adipose tissue inflammation caused by obesity . For example, resolvin D1 exerts anti-inflammatory properties at nanomolar concentrations, whereas the
obesity 58370 micromolar level, suggesting that resolvin D1 may be more effective for ameliorating inflammation in obesity [[204]]. Moreover, deletion of D6D lowers the conversion of ALA to EPA [[59]]. Expression of D6D is
obesity 61916 umbilical plasma concentration was 4.6% ± 1.2%. 2. DHA + EPA = lower skin fold thickness and odds of obesity . 3. Maternal plasma DHA + EPA not associated with child adiposity.[[7]]Healthy men1. Fish diet group:
obesity 67130 or continuous application with osmotic (Alzet) pumps (∼120) for 15 days1. Genetic and diet-induced obesity decreases adipose tissue n-3 PUFA–derived lipid mediators 17-HDHA and PD1.2. Adipose tissue 17-HDHA
obesity 67541 PUFA linked to increase SPMs and their precursors in adipose tissue.5. Treatment with 17-HDHA reduces obesity -induced adipose tissue inflammation.6. Treatment with 17-HDHA improves metabolic regulation in obesity.[[121]]RatWistar
obesity 67644 obesity-induced adipose tissue inflammation.6. Treatment with 17-HDHA improves metabolic regulation in obesity .[[121]]RatWistar rats1. Control (sucrose replaced by starch)2. Sucrose-rich (SRD) diet (corn oil, 8/100

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