Background and aimsLow-carbohydrate diets (LCD) and low-fat diets (LFD) have shown beneficial effects on the management of obesity. Epidemiological studies were conducted to compare the effects of the two diets. However, the results were not always consistent. This study aimed to conduct a meta-analysis to compare the long-term effects of LCD and LFD on metabolic risk factors and weight loss in overweight and obese adults.MethodsWe performed a systematic literature search up to 30 March, 2022 in PubMed, EMBASE, and Cochrane Library. The meta-analysis compared the effects of LCD (carbohydrate intake ≤ 40%) with LFD (fat intake < 30%) on metabolic risk factors and weight loss for ≥6 months. Subgroup analyses were performed based on participant characteristics, dietary energy intake, and the proportions of carbohydrates.Results33 studies involving a total of 3,939 participants were included. Compared with participants on LFD, participants on LCD had a greater reduction in triglycerides (–0.14 mmol/L; 95% CI, –0.18 to –0.10 mmol/L), diastolic blood pressure (–0.87 mmHg; 95% CI, –1.41 to –0.32 mmHg), weight loss (–1.33 kg; 95% CI, –1.79 to –0.87 kg), and a greater increase in high-density lipoprotein cholesterol (0.07 mmol/L; 95% CI, 0.06 to 0.09 mmol/L) in 6–23 months. However, the decrease of total cholesterol (0.14 mmol/L; 95% CI, 0.07 to 0.20 mmol/L) and low-density lipoprotein cholesterol (0.10 mmol/L; 95% CI, 0.06 to 0.14 mmol/L) was more conducive to LFD in 6–23 months. There was no difference in benefits between the two diets after 24 months. Subgroup analyses showed no significant difference in the reduction of total cholesterol, low-density lipoprotein cholesterol, and blood pressure between the two diets in participants with diabetes, hypertension, or hyperlipidemia.ConclusionThe results suggest that LCD and LFD may have specific effects on metabolic risk factors and weight loss in overweight and obese adults over 6 months. At 24 months, the effects on weight loss and improvement of metabolic risk factors were at least the same. These indicated that we might choose different diets to manage the overweight and obese subjects. However, the long-term clinical efficacy and effects of various sources of carbohydrates or fat in the two diets need to be studied in the future.
Activation of the angiotensin II type 2 receptor (AT2R) induces diuresis and natriuresis. Increased expression or/and activity of G protein-coupled receptor kinase 4 (GRK4) or genetic variants (e.g., GRK4γ142V) cause sodium retention and hypertension. Whether GRK4 plays a role in the regulation of AT2R in the kidney remains unknown. In this study, we found that spontaneously hypertensive rats (SHRs) had increased AT2R phosphorylation and impaired AT2R-mediated diuretic and natriuretic effects, as compared with normotensive Wistar-Kyoto (WKY) rats. The regulation by GRK4 of renal AT2R phosphorylation and function was studied in human (h) GRK4γ transgenic mice. hGRK4γ142V transgenic mice had increased renal AT2R phosphorylation and impaired AT2R-mediated natriuresis, relative to hGRK4γ wild-type (WT) littermates. These were confirmed in vitro; AT2R phosphorylation was increased and AT2R-mediated inhibition of Na+-K+-ATPase activity was decreased in hGRK4γ142V, relative to hGRK4γ WT-transfected renal proximal tubule (RPT) cells. There was a direct physical interaction between renal GRK4 and AT2R that was increased in SHRs, relative to WKY rats. Ultrasound-targeted microbubble destruction of renal GRK4 decreased the renal AT2R phosphorylation and restored the impaired AT2R-mediated diuresis and natriuresis in SHRs. In vitro studies showed that GRK4 siRNA reduced AT2R phosphorylation and reversed the impaired AT2R-mediated inhibition of Na+-K+-ATPase activity in SHR RPT cells. Our present study shows that GRK4, at least in part, impairs renal AT2R-mediated diuresis and natriuresis by increasing its phosphorylation; inhibition of GRK4 expression and/or activity may be a potential strategy to improve the renal function of AT2R.
Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) are essential for the development of hypertension. Insulin has been identified to promote VSMC proliferation and migration; resveratrol has been shown to have protective effects against cardiovascular diseases. This study aimed to investigate the effect of resveratrol on insulin-induced VSMC proliferation and migration and its potential mechanism. VSMC proliferation was measured by Cell Counting Kit-8 (CCK-8), cell counting method, and 5-ethynyl-2′-deoxyuridine (EdU) incorporation assay. Cell migration was detected by wound healing assay and transwell method. Expression of silent information regulator of transcription 1 (SIRT1) and phosphorylation levels of signaling molecules, such as phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt), in VSMCs were detected by Western blotting. Resveratrol (25-150 μM) was found to inhibit insulin-induced VSMC proliferation. Pretreatment with 100 μM resveratrol reduced insulin (100 nM)-mediated VSMC migration. LY294002, an inhibitor of PI3K, inhibited the stimulatory effect of insulin (100 nM) on the proliferation of VSMCs. Treatment with resveratrol also decreased insulin-induced stimulatory effect on PI3K and Akt phosphorylation levels. Moreover, resveratrol treatment increased SIRT1 protein expression in VSMCs. A SIRT1 inhibitor, EX527, reversed the inhibitory effect of resveratrol on insulin-induced VSMC proliferation and migration and activation of PI3K and Akt phosphorylation levels. In conclusion, our study revealed that treatment with resveratrol inhibited insulin-mediated VSMC proliferation and migration, possibly by activating SIRT1 and downregulating the PI3K/AKT pathway.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.