scholarly journals Pomegranate seed oil consumption during a period of high-fat feeding reduces weight gain and reduces type 2 diabetes risk in CD-1 mice

2008 ◽  
Vol 102 (1) ◽  
pp. 54-59 ◽  
Author(s):  
Brian K. McFarlin ◽  
Kelley A. Strohacker ◽  
Michael L. Kueht
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Seed Oil ◽  
Low Grade ◽  
High Fat ◽  
Pomegranate Seed Oil ◽  
Glucose Sensitivity ◽  
Pomegranate Seed ◽  
Low Grade Inflammation

The health benefits of pomegranate consumption have recently received considerable scientific focus, with most studies examining fruit and/or juice consumption. Pomegranate seed oil (POMo) is a rich source of 9-cis, 11-trans conjugate linolenic acid (CLA), which may offset the side-effects associated with weight gain. Male, wild-type CD-1 mice were divided into one of three groups (twenty per group): high-fat (HF), HF+seed oil (HF+POMo) or lean control (LN). In HF and HF+POMo, mice were provided access ad libitum to a high-fat chow (60 % of energy from fat). HF+POMo was supplemented with 61·79 mg POMo/d. LN consumed a restricted low-fat (10 % of energy from fat) chow to maintain body weight within 5 % of initial weight. Plasma was analysed for biomarkers associated with cholesterol profile (total cholesterol, HDL and TAG), glucose sensitivity (glucose and insulin), adipose tissue accumulation (leptin and adiponectin) and systemic low-grade inflammation (C-reactive protein and haptoglobin). The key findings of this study were that weight gain was associated with an increase in biomarkers of cholesterol profile, glucose sensitivity, adipose tissue accumulation and systemic low-grade inflammation (P < 0·05). POMo only altered body weight accumulation, final body weight, leptin, adiponectin and insulin (P < 0·05). We found that despite a similar level of energy intake, HF mice had a greater concentration of leptin and a lower concentration of adiponectin compared to HF+POMo mice. POMo intake was associated with an improvement in insulin sensitivity, suggesting that risk of developing type 2 diabetes may have been reduced; however, CVD risk did not change.

scholarly journals Cardiovascular benefits of GLP-1 agonists in type 2 diabetes: a comparative review

2018 ◽  
Vol 132 (15) ◽  
pp. 1699-1709 ◽  
Author(s):  
James G. Boyle ◽  
Rachel Livingstone ◽  
John R. Petrie
Keyword(s):  
Type 2 Diabetes ◽  
Body Weight ◽  
Ldl Cholesterol ◽  
Microvascular Complications ◽  
Standard Of Care ◽  
Low Grade ◽  
Glucose Lowering ◽  
Comparative Review ◽  
Low Grade Inflammation

Type 2 diabetes (T2D) carries risks of both cardiovascular (CV) (myocardial infarction, stroke, and peripheral vascular disease) and microvascular (retinopathy/nephropathy/neuropathy) complications. Glucose-lowering is an effective strategy for preventing microvascular complications, but the extent to which it can reduce CV complications is less certain. Glucagon-like peptide-1 (GLP-1) agonists are potent glucose-lowering agents but also have potentially beneficial effects on other traditional (body weight, blood pressure (BP), and LDL cholesterol) and non-traditional risk factors (low grade inflammation and endothelial dysfunction). The results of four large CV outcome trials with GLP-1 agonists are now available. These have compared lixisenatide (ELIXA), liraglutide (LEADER), semaglutide (SUSTAIN-6), and long-acting exenatide (EXSCEL) with placebo and standard of care over 2–4 years; four others (including with dulaglutide and albiglutide) are ongoing. LEADER and SUSTAIN-6 have demonstrated reductions in rates of major adverse CV events with active GLP-1 treatment but ELIXA and EXSCEL have not. In this review, we discuss the mechanisms by which GLP-1 receptor agonists act on the CV system and the design and conduct of these trials. Contrary to the assertions that (a) all GLP-1 agonists reduce CV disease in T2D but to different extents or (b) the magnitude of CV protection is predominantly related to glucose-lowering, we argue that CV benefit is specific to agents that provide longer acting agonism at the GLP-1 receptor. The mechanisms involve reduction in body weight and BP, and lowering of LDL-cholesterol and glucose, but pleiotropic effects—including suppression of low grade inflammation, vasodilation, and natriuresis—are also likely relevant.

scholarly journals Estradiol and high fat diet associate with changes in gut microbiota in female ob/ob mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kalpana D. Acharya ◽  
Xing Gao ◽  
Elizabeth P. Bless ◽  
Jun Chen ◽  
Marc J. Tetel
Keyword(s):  
Weight Gain ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Energy Homeostasis ◽  
Low Grade ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Increased Risk ◽  
17Β Estradiol ◽  
Low Grade Inflammation

AbstractEstrogens protect against diet-induced obesity in women and female rodents. For example, a lack of estrogens in postmenopausal women is associated with an increased risk of weight gain, cardiovascular diseases, low-grade inflammation, and cancer. Estrogens act with leptin to regulate energy homeostasis in females. Leptin-deficient mice (ob/ob) exhibit morbid obesity and insulin resistance. The gut microbiome is also critical in regulating metabolism. The present study investigates whether estrogens and leptin modulate gut microbiota in ovariectomized ob/ob (obese) or heterozygote (lean) mice fed high-fat diet (HFD) that received either 17β-Estradiol (E2) or vehicle implants. E2 attenuated weight gain in both genotypes. Moreover, both obesity (ob/ob mice) and E2 were associated with reduced gut microbial diversity. ob/ob mice exhibited lower species richness than control mice, while E2-treated mice had reduced evenness compared with vehicle mice. Regarding taxa, E2 was associated with an increased abundance of the S24-7 family, while leptin was associated with increases in Coriobacteriaceae, Clostridium and Lactobacillus. Some taxa were affected by both E2 and leptin, suggesting these hormones alter gut microbiota of HFD-fed female mice. Understanding the role of E2 and leptin in regulating gut microbiota will provide important insights into hormone-dependent metabolic disorders in women.

scholarly journals Effects of pomegranate seed oil on metabolic state of patients with Type 2 diabetes mellitus

2016 ◽  
Vol 7 (1) ◽  
pp. 124 ◽  
Author(s):  
Parvin Mirmiran ◽  
Zahra Faghihimani ◽  
Golbon Sohrab ◽  
Bijan Iraj ◽  
Elham Faghihimani
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Seed Oil ◽  
Metabolic State ◽  
Pomegranate Seed Oil ◽  
Pomegranate Seed

scholarly journals Polyphenols from Passiflora ligularis Regulate Inflammatory Markers and Weight Gain

2021 ◽  
Vol 12 (1) ◽  
pp. 36-45
Author(s):  
Jaime Angel-Isaza ◽  
Juan Carlos Carmona-Hernandez ◽  
William Narváez-Solarte ◽  
Clara Helena Gonzalez-Correa
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Wistar Rats ◽  
Adult Population ◽  
Control Group ◽  
Chow Diet ◽  
Low Grade ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Low Grade Inflammation

Abstract Weight-related disorders affect more than half of the adult population worldwide; they are also concomitant with a state of chronic low-grade inflammation manifesting in abnormal cytokine production. The present study evaluated the effect of polyphenol and flavonoid extract from Passiflora ligularis (granadilla) on low-grade inflammation and body weight in overweight Wistar rats. To induce weight-gain, rats were fed a chow diet with 30% sucrose water and supplemented with 2.0, 2.5, and 3.0 g/L polyphenol extracts (n = 16). The design was a 3 +1 factorial model performed for 42 days (granadilla polyphenols, 3 levels of supplementation, and 1 control group). In addition to total polyphenol and total flavonoid content, the major identified and quantified polyphenol, via UHPLC, was ferulic acid. Interleukin 6 (IL-6), and cytokine tumor necrosis factor-alpha (TNF-α) were evaluated in serum. A decline in the concentration of TNF-α and in weight-gain was found in P. ligularis (granadilla) groups treated with the 2.5 g/L dose. Consumption of polyphenol extracts from granadilla inhibits interleukin-activity as an indicator of inflammation and aids in body-weight control, considering similar food intake, in overweight Wistar rats.

scholarly journals Mice lacking NOX2 are hyperphagic and store fat preferentially in the liver

2014 ◽  
Vol 306 (12) ◽  
pp. E1341-E1353 ◽  
Author(s):  
Sheila R. Costford ◽  
Jason Castro-Alves ◽  
Kenny L. Chan ◽  
Liane J. Bailey ◽  
Minna Woo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Hepatic Steatosis ◽  
Immune Cells ◽  
Low Grade ◽  
High Fat ◽  
Insulin Resistant ◽  
Nadph Oxidase Complex ◽  
Low Grade Inflammation ◽  
Fat Feeding

Chronic low-grade inflammation is an important contributor to the development of insulin resistance, a hallmark of type 2 diabetes mellitus (T2DM). Obesity and high-fat feeding lead to infiltration of immune cells into metabolic tissues, promoting inflammation and insulin resistance. We hypothesized that macrophages from mice lacking NOX2 ( Cybb), an essential component of the NADPH oxidase complex highly expressed in immune cells and associated with their inflammatory response, would be less inflammatory and that these mice would be protected from the development of high-fat-induced insulin resistance. Bone marrow-derived macrophages from NOX2 knockout (NOX2-KO) mice expressed lower levels of inflammatory markers ( Nos2, Il6); however, NOX2-KO mice were hyperphagic and gained more weight than wild-type (WT) mice when fed either a chow or a high-fat (HF) diet. Surprisingly, NOX2-KO mice stored less lipid in epididymal white adipose tissue but more lipid in liver and had higher indexes of liver inflammation and macrophage infiltration than WT mice. Contrary to our hypothesis, HF-fed NOX2-KO mice were hyperinsulinemic and more insulin resistant than HF-fed WT mice, likely as a result of their higher hepatic steatosis and inflammation. In summary, NOX2 depletion promoted hyperphagia, hepatic steatosis, and inflammation with either normal or high-fat feeding, exacerbating insulin resistance. We propose that NOX2 participates in food intake control and lipid distribution in mice.

scholarly journals LETTER TO THE EDITOR: Pomegranate Juice Intake and Cardiovascular Health

2013 ◽  
Vol 5 (1) ◽  
pp. 27-28
Author(s):  
Venetia Notara ◽  
Demosthenes B. Panagiotakos
Keyword(s):  
Risk Factors ◽  
Type 2 Diabetes ◽  
Protective Effect ◽  
Clinical Studies ◽  
Seed Oil ◽  
Pomegranate Juice ◽  
Cvd Risk ◽  
Pomegranate Seed Oil ◽  
Pomegranate Seed

The public health burden of cardiovascular diseases (CVDs) is substantial. According to the World Health Organization report “The Global Burden of Disease” 2013 Update, heart diseases are expected to take the second place in the rank order of disease and injury burden by the year 2030 [1]. More than 50% reduction of CVD mortality is attributable to favourable changes in risk factors, while 43% to new medical and surgical treatment [2,3]. Extended research data has indicated that diet is one of the modifiable risk factors that has been substantially related to CVD prevention, through several serum antioxidant and antithrombotic mechanisms. Emphasis has been given to the daily consumption of fruits and vegetables due to the high source, among others, of phenolic acids and flavonoids that are known for their antioxidant properties [4]. In the most recent years, laboratory and clinical studies have examined the health benefits of pomegranate juice consumption, which have demonstrated its protective effect against the progression of atherosclerosis [5]. Pomegranate fruit has very high levels of antioxidants- mainly polyphenols- as well as tannins and anthocyanins, which seem to improve vascular function and modulation of inflammation. In a recent study conducted in a sample of people with hypertension, it has been observed that pomegranate juice can significantly lower blood pressure even in a 2-week intake of fresh juice [6]. Polyphenolic flavonoids are powerful antioxidants which can inhibit the harmful oxidation effect of low-density LDL and consequently restrain atherosclerosis development [7]. Pomegranate seed oil consumption seems to be associated with an improvement in insulin sensitivity, posing an additional protective effect in the development of type 2 diabetes [8]. However, in the same study the CVD – related risk did not change, while other studies did not show a decrease in the type 2 diabetes risk or a reduction in the lipid peroxidation among healthy controls, too [5,9]. It should also be mentioned, that pomegranate seed oil does not have polyhpenols. Despite the fact that dietary flavonoids seem to have a potential effect on the reduction of CVD risk, the question of whether isolated polyphenols are the responsible compounds for vascular health still remains unanswered. Long-term clinical studies exploring the bioactive compounds of various types of fruits are required to determine the potential synergistic effects of polyphenols and the dose-response relationships [10]. Additionally, the impact of pomegranate polyphenol extracts among healthy and high CVD risk subjects needs further investigation.

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