Literature showed that soluble fiber has beneficial effects on cardiometabolic risk factors and leptin and adiponectin serum levels. Our aim in this meta-analysis was to determine the effect of soluble fiber supplementation on leptin and adiponectin serum levels. A systematic search was conducted using PubMed, Scopus, and ISI Web of Science for eligible trials up to December 2021. A random-effects model was used to pool calculated effect sizes. Our analysis showed that soluble fiber supplementation did not significantly affect adiponectin (standardized mean difference [SMD], −0.49 Hedges’s, 95% confidence interval [CI], −1.20, 0.21, p value = 0.167; I2 = 95.4, p value < 0.001) and leptin (SMD, −0.8 Hedges’s, 95% CI, −1.70, 0.08, p value = 0.076; I2 = 94.6, p value < 0.001) concentrations in comparison with placebo. However, in the subgroup, soluble fiber supplementation had a significant improvement in leptin concentration in overweight and obese patients (SMD, −0.22 Hedges’s, 95% CI, −0.43, −0.01, p value = 0.048) and a non-significant beneficial effect in adiponectin level in female (SMD, 0.29 Hedges’s, 95% CI, −0.13, 0.71, p value = 0.183) and diabetic patients (SMD, 0.32 Hedges’s, 95% CI, −0.67, 1.32, p value = 0.526). A non-linear association between soluble fiber dosage and adiponectin (pnon-linearity < 0.001) was observed. Soluble fiber supplementation could not change the circulatory leptin and adiponectin levels. However, beneficial effects were seen in overweight and obese leptin, and increases in adiponectin may also be observed in female and diabetic patients. Further studies are needed to confirm this results.
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Adiponectin, and leptin are adipose tissue derived hormones affecting metabolic status. This study aimed to investigate the relationship between circulating adiponectin and leptin levels, and cardiometabolic parameters by obesity status among healthy women without metabolic disease. Finally 141 participants were included in the analyses and categorized into three groups by their body mass index (kg/m2) (normal weight: 18.5 ≤ body mass index [BMI] < 23.0, n=65; overweight: 23.0 ≤ BMI < 25.0, n=26; obesity: 25.0 ≤ BMI, n=50). Overweight and obesity groups were older, and had significantly higher levels of adiposity, blood pressure, fasting glucose, triglyceride, and high sensitivity C-reactive protein (hs-CRP), and lower levels of high density lipoprotein (HDL)-cholesterol than normal weight group. Circulating leptin levels, and leptin to adiponectin ratio were highest in obesity group, but circulating adiponectin levels were not statistically different among the three groups. Circulating leptin levels were negatively correlated with adiponectin levels, and leptin to adiponectin ratio. In addition, leptin levels were positively correlated with waist circumference, systolic blood pressure, insulin resistance, and hs-CRP, and negatively with HDL-cholesterol. However, circulating adiponectin levels were negatively correlated only with waist circumference, and hs-CRP. These patterns were retained after adjusted for confounding factors such as age, smoking and drinking habits, menopausal status and total calorie intake. In conclusion, circulating adiponectin and leptin levels according to obesity status were differently observed among healthy women, and circulating leptin levels may be a more sensitive parameter for cardiometabolic risk in healthy women.
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Circadian disruption causes obesity and other metabolic disorders. There is no research considering the role of Cryptochromes (Cry) 1 body clock gene and major dietary patterns on serum leptin level and obesity. We aimed to investigate the interaction between
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The defective satiation signaling may contribute to the etiology of obesity. We investigated how dietary modification during maternal (pregnancy and lactation) and post-weaning affects obesity, insulin resistance (IR) and hypothalamic appetite responses in offspring in adulthood. Pregnant female SD rats were randomly allocated to either maternal high-fat diet (43% energy from fat) or control diet (12% energy from fat) until the end of suckling. After weaning for additional 4 weeks, half of the offsprings were continuously fed the same diet as the dam (C-C and H-H groups); the remainder received the counterpart diet (C-H and H-C groups). The long-term high-fat diet during maternal and post-weaning period (H-H group) led to susceptibility to obesity and IR through the significant increases of hypothalamic orexigenic genes compared to the maternal and post-weaning control diet group (C-C group). In contrast, the hypothalamic expression levels of anorexigenic genes, apolipoprotein E, leptin receptor, and activated signal transducer and activator of transcription protein 3 were significantly lower in H-H group with elevations in circulating insulin and leptin and body fat mass. However, dietary changes after weaning (H-C and C-H groups) partially modified these conditions. These results suggest that maternal and post-weaning diet conditions can potentially disrupt hypothalamic neuronal signal irrelevantly, which is essential for leptin's regulation of energy homeostasis and induce the risk of offspring to future metabolic disorders.
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The present study was conducted to compare serum leptin and insulin resistance levels between Korean postmenopausal long-term semi-vegetarians and non-vegetarians. Subjects of this study belonged to either a group of postmenopausal vegetarian women (n = 54), who maintained a semi-vegetarian diet for over 20 years or a group of non-vegetarian controls. Anthropometric characteristics, serum leptin, serum glucose, serum insulin, insulin resistance (HOMA-IR; Homeostasis Model Assessment of Insulin Resistance), and nutrient intake were compared between the two groups. The vegetarians showed significantly lower body weight (p < 0.01), body mass index (p < 0.001), percentage (%) of body fat (p < 0.001), and serum levels of leptin (p < 0.05), glucose (p < 0.001), and insulin (p < 0.01), than the non-vegetarians. The HOMA-IR of the vegetarians was significantly lower than that of the non-vegetarians (p < 0.01) after adjustment for the % of body fat. A long-term vegetarian diet might be related to lower insulin resistance independent of the % of body fat in postmenopausal women.
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Understanding the relationship between energy nutrients compositions in a diet and appetite-controlling substances is essential for providing sound advice to anyone attempting to control body weight. Appetite is known to be affected by various hormones, ghrelin and peptide tyrosine-tyrosine (PYY), which are related to the compositions of a diet. The purpose of this study was to investigate the effects of compositions of energy nutrients in the diet on the levels of postprandial appetite-related hormones and satiety in healthy adult women. Ten subjects (BMI: 18.5-22.9 kg/m2) were recruited and assigned to three iso-coloric breakfast meals with different compositions of energy nutrients, regular meal (RM, CHO: 60%, Pro: 20%, Fat: 20%), high protein meal (HPM, CHO: 30%, Pro: 50%, Fat: 20%), and high fat meal (HFM, CHO: 30%, Pro: 20%, Fat: 50%). Blood levels of ghrelin, PYY, insulin and leptin and satiety were assessed at baseline, 30, 60, 90, 120, and 180 min following the consumption of each meal. There was no significant difference in the fasting blood hormones among the subjects taking each meals at baseline. Blood levels of ghrelin and insulin changed significantly following the consumption of each meal (p<0.05) over time, however no significant difference was shown between experimental meals until 180 min. Blood levels of PYY and leptin were not changed following the ingestion of each meals. In conclusion, the composition of energy nutrients in a diet had no effect on the postprandial plasma levels of ghrelin, PYY, insulin and leptin as well as satiety in healthy adult women.
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