Obesity is a leading global health problem contributing to various chronic diseases, including type II diabetes mellitus (T2DM). The aim of this study was to investigate whether blueberries, yoghurt, ...and their respective bioactive components, Cyanidin-3-O-β-glucoside (C3G) and peptides alone or in combinations, alter the expression of genes related to glucose metabolism in skeletal muscles from diet-induced obese mice. In extensor digitorum longus (EDL), yoghurt up-regulated the expression of activation of 5’adenosine monophosphate-activated protein kinase (AMPK), insulin receptor substrate-1 (IRS-1), phosphatidylinositol-3 kinase (PI3K) and glucose transporter 4 (GLUT4), and down-regulated the expression of angiotensin II receptor type 1 (AGTR-1). The combination of blueberries and yoghurt down-regulated the mRNA expression of AGTR-1 and Forkhead box protein O1 (FoxO1) in the EDL. Whereas the combination of C3G and peptides down-regulated AGTR-1 and up-regulated GLUT4 mRNA expression in the EDL. In the soleus, blueberries and yoghurt alone, and their combination down-regulated AGTR-1 and up-regulated GLUT4 mRNA expression. In summary blueberries and yoghurt, regulated multiple genes associated with glucose metabolism in skeletal muscles, and therefore may play a role in the management and prevention of T2DM.
Linoleic acid and the pathogenesis of obesity Naughton, Shaan S.; Mathai, Michael L.; Hryciw, Deanne H. ...
Prostaglandins & other lipid mediators,
September 2016, 2016-09-00, 20160901, Volume:
125
Journal Article
Peer reviewed
•Worldwide linoleic acid (LA) intakes have increased due to nutrition transitions.•LA intake exceeds what is required and may have detrimental health effects.•Excessive LA intake has been implicated ...in the development of obesity.•Excessive LA may contribute to the chronic inflammatory state found in obesity.•Genetics and maternal diet influence the effect of LA on obesity and inflammation.
The modern Western diet has been consumed in developed English speaking countries for the last 50 years, and is now gradually being adopted in Eastern and developing countries. These nutrition transitions are typified by an increased intake of high linoleic acid (LA) plant oils, due to their abundance and low price, resulting in an increase in the PUFA n-6:n-3 ratio. This increase in LA above what is estimated to be required is hypothesised to be implicated in the increased rates of obesity and other associated non-communicable diseases which occur following a transition to a modern Westernised diet. LA can be converted to the metabolically active arachidonic acid, which has roles in inducing inflammation and adipogenesis, and endocannabinoid system regulation. This review aims to address the possible implications of excessive LA and its metabolites in the pathogenesis of obesity.
Adipocytes secrete a number of bioactive adipokines that activate a variety of cell signaling pathways in central and peripheral tissues. Obesity is associated with the altered production of many ...adipokines and is linked to a number of pathologies. As an increase in body weight is directly associated with an increased risk for developing chronic kidney disease (CKD), there is significant interest in the link between obesity and renal dysfunction. Altered levels of the adipokines leptin, adiponectin, resistin, and visfatin can decrease the glomerular filtration rate and increase albuminuria, which are pathophysiological changes typical of CKD. Specifically, exposure of the glomerulus to altered adipokine levels can increase its permeability, fuse the podocytes, and cause mesangial cell hypertrophy, all of which alter the glomerular filtration rate. In addition, the adipokines leptin and adiponectin can act on tubular networks. Thus, adipokines can act on multiple cell types in the development of renal pathophysiology. Importantly, most studies have been performed using in vitro models, with future studies in vivo required to further elucidate the specific roles that adipokines play in the development and progression of CKD.
Emerging research has highlighted the importance of leptin in fetal growth and development independent of its essential role in the maintenance of hunger and satiety through the modulation of ...neuropeptide Y and proopiomelanocortin neurons. Alterations in maternal-placental-fetal leptin exchange may modify the development of the fetus and contribute to the increased risk of developing disease in adulthood. In addition, leptin also plays an important role in reproductive functions, with plasma leptin concentrations rising in pregnant women, peaking during the third trimester. Elevated plasma leptin concentrations occur at the completion of organogenesis, and research in animal models has demonstrated that leptin is involved in the development and maturation of a number of organs, including the heart, brain, kidneys, and pancreas. Elevated maternal plasma leptin is associated with maternal obesity, and reduced fetal plasma leptin is correlated with intrauterine growth restriction. Alterations in plasma leptin during development may be associated with an increased risk of developing a number of adulthood diseases, including cardiovascular, metabolic, and renal diseases via altered fetal development and organogenesis. Importantly, research has shown that leptin antagonism after birth significantly reduces maturation of numerous organs. Conversely, restoration of the leptin deficiency after birth in growth-restricted animals restores the offspring's body weight and improves organogenesis. Therefore, leptin appears to play a major role in organogenesis, which may adversely affect the risk of developing a number of diseases in adulthood. Therefore, greater understanding of the role of leptin during development may assist in the prevention and treatment of a number of disease states that occur in adulthood.
Maternal nutrition plays a critical role in fetal development and can influence adult onset of disease. Linoleic acid (LA) and alpha‐linolenic acid (ALA) are major omega‐6 (n‐6) and n‐3 ...polyunsaturated fatty acids (PUFA), respectively, that are essential in our diet. LA and ALA are critical for the development of the fetal neurological and immune systems. However, in recent years, the consumption of n‐6 PUFA has increased gradually worldwide, and elevated n‐6 PUFA consumption may be harmful to human health. Consumption of diets with high levels of n‐6 PUFA before or during pregnancy may have detrimental effects on fetal development and may influence overall health of offspring in adulthood. This review discusses the role of n‐6 PUFA in fetal programming, the importance of a balance between n‐6 and n‐3 PUFAs in the maternal diet, and the need of further animal models and human studies that critically evaluate both n‐6 and n‐3 PUFA contents in diets.
Cystic fibrosis (CF), the result of mutations in the CF transmembrane conductance regulator (CFTR), causes essential fatty acid deficiency. The aim of this study was to characterize fatty acid ...handling in two rodent models of CF; one strain which harbors the loss of phenylalanine at position 508 (Phe508del) in CFTR and the other lacks functional CFTR (510X). Fatty acid concentrations were determined using gas chromatography in serum from Phe508del and 510X rats. The relative expression of genes responsible for fatty acid transport and metabolism were quantified using real-time PCR. Ileal tissue morphology was assessed histologically. There was an age-dependent decrease in eicosapentaenoic acid and the linoleic acid:α-linolenic acid ratio, a genotype-dependent decrease in docosapentaenoic acid (n-3) and an increase in the arachidonic acid:docosahexaenoic acid ratio in Phe508del rat serum, which was not observed in 510X rats. In the ileum,
mRNA was increased in Phe508del rats but decreased in 510X rats. Further,
,
,
and
mRNA were increased in Phe508del rats only. As assessed by Sirius Red staining, collagen was increased in Phe508del and 510X ileum. Thus, CF rat models exhibit alterations in the concentration of circulating fatty acids, which may be due to altered transport and metabolism, in addition to fibrosis and microscopic structural changes in the ileum.
•Body weight and fat mass.•Glucose metabolism and insulin signalling.•Lipid metabolism.•Inflammation.•Adipocytokine profile.
Recent experimental and clinical studies suggest that consumption of ...blueberry products has potential health benefits in ameliorating the development of obesity and its related comorbidities, including type 2 diabetes (T2D) and chronic inflammation. Blueberry fruits are enriched with numerous bioactive components such as vitamins, phenolic acid and anthocyanins which could contribute to these protective effects. Possible mechanisms by which blueberries exert their beneficial properties include counteracting oxidative stress, regulating glucose metabolism, improving lipid profile, and lowering inflammatory cytokine levels in animal models and preliminary human trials. This review focuses on the potential role of blueberries as a functional food in the prevention and treatment of obesity and its comorbidities. Although the current evidence is promising, further randomized controlled studies in the longer term are needed to evaluate the role of blueberries and blueberry extracts to support human health.
Diet-induced obesity (DIO) is a contributor to co-morbidities, resulting in alterations in hormones, lipids, and low-grade inflammation, with the cannabinoid type 2 receptor (CB2) contributing to the ...inflammatory response. The effects of modulating CB2 with pharmacological treatments on inflammation and adaptations to the obese state are not known. Therefore, we aimed to investigate the molecular mechanisms in adipose tissue of CB2 agonism and CB2 antagonism treatment in a DIO model. Male Sprague Dawley rats were placed on a high-fat diet (HFD) (21% fat) for 9 weeks, then received daily intraperitoneal injections with a vehicle, AM630 (0.3 mg/kg), or AM1241 (3 mg/kg), for a further 6 weeks. AM630 or AM1241 treatment in DIO rats did not alter their body weight, food intake, or liver weight, and it had no effect on their numerous circulating cytokines or peri-renal fat pad mass. AM1241 decreased heart weight and BAT weight; both treatments (AM630 or AM1241) decreased plasma leptin levels, while AM630 also decreased plasma ghrelin and GLP-1 levels. Both treatments decreased Adrb3 and TNF-α mRNA levels in eWAT and TNF-α levels in pWAT. AM630 treatment also decreased the mRNA levels of Cnr2, leptin, and Slc2a4 in eWAT. In BAT, both treatments decreased leptin, UCP1, and Slc2a4 mRNA levels, with AM1241 also decreasing Adrb3, IL1β, and PRDM16 mRNA levels, and AM630 increasing IL6 mRNA levels. In DIO, CB2 agonist and CB2 antagonist treatment reduces circulating leptin in the absence of weight loss and modulates the mRNA responsible for thermogenesis.
Summary
Edible portions of Leucopogon parviflorus, Arthropodium strictum, Carpobrotus rossii, Rhagodia candolleana, Typha orientalis, Correa alba, Dianella revoluta and Acacia longifolia were ...collected in 2017 and 2019 from Warrnambool, Victoria Australia, and studied for phenolics and proximate composition. The plant species recorded consistent antioxidant activity with no nutritional alterations. Except for A. longifolia, total phenolic contents (TPC) were higher in 2019 than 2017 (P < 0.05). All the plant species contained Ca, Mg, Na and K. Except for betanin, isolated from R. candolleana (700 mg L−1) and C. rossii (244 mg L−1), higher quantities of polyphenols were extractable in methanol than water (P < 0.05). The plant fatty acid composition was predominantly palmitic, oleic and linoleic acids with A. longifolia containing 44% linoleic acid. While the plant nutrients and fatty acids were fairly stable, TPCs, some of the minerals and polyphenols varied between the years.
Proximate and phenolic composition of selected native Australian food plants.
Mice lacking the Jak tyrosine kinase member Tyk2 become progressively obese due to aberrant development of Myf5+ brown adipose tissue (BAT). Tyk2 RNA levels in BAT and skeletal muscle, which shares a ...common progenitor with BAT, are dramatically decreased in mice placed on a high-fat diet and in obese humans. Expression of Tyk2 or the constitutively active form of the transcription factor Stat3 (CAStat3) restores differentiation in Tyk2−/− brown preadipocytes. Furthermore, Tyk2−/− mice expressing CAStat3 transgene in BAT also show improved BAT development, normal levels of insulin, and significantly lower body weights. Stat3 binds to PRDM16, a master regulator of BAT differentiation, and enhances the stability of PRDM16 protein. These results define Tyk2 and Stat3 as critical determinants of brown fat lineage and suggest that altered levels of Tyk2 are associated with obesity in both rodents and humans.
► Mice that do not express the Jak kinase Tyk2 become obese ► The expression of Tyk2 is decreased in obese mice and obese humans ► Expression of Tyk2 is required for differentiation of brown adipose tissue ► Expression of constitutively active Stat3 transgene reverses obesity in Tyk2−/− mice
PDF
