Background This study investigated associations between dairy intake and chronic metabolic diseases (CMDs), and evaluated possible dose‐response relationships in Chinese. Methods This cross‐sectional study included 6073 adults aged ≥18 years from China. General characteristics were gathered using a validated dietary questionnaire. Multivariable logistic regression analyses investigated associations between dairy intake and chronic metabolic diseases (CMDs) (overweight/obesity, obesity, central obesity, and hyperlipidemia). Restricted cubic spline models explored dose‐response relationships between dairy intake and CMDs, and possible dairy intake in the prevention of CMDs. Structural equation modeling explored the potential mechanisms of the effects of dairy intake on CMDs. Results Significant inverse associations were found between dairy intake and overweight/obesity, obesity, central obesity, and hyperlipidemia, with odds ratios (ORs) of 0.66 (95% confidence interval [CI] 0.56‐0.79), 0.63 (95% CI 0.47‐0.85), 0.71 (95% CI 0.60‐0.85), and 0.81 (95% CI 0.56‐1.17), respectively (P < 0.05 for all). The intake of yogurt, milk, and total dairy to prevent CMDs differed according to age group (16‐74, 29‐187, and 159‐269 mL/d, respectively, in the entire group; 69‐110, 59‐152, and 138‐167 mL/d, respectively, in the young group, ≤ 44 years; 9‐58, 57‐149, and 117‐145 mL/d, respectively, in the middle‐aged group, 45‐59 years; and 23‐59 mL/d yogurt only in the old group, ≥ 60 years). Structural equation modeling showed that dairy intake could reduce body mass index and waist circumference by regulating carbohydrate, fat, protein, and total energy. Conclusions Dairy intake was inversely associated with the prevalence of overweight, obesity, central obesity, and hyperlipidemia, and the optimal range of dairy intake differed with age. The beneficial effects of dairy intake in preventing CMDs could involve regulation of carbohydrate, fat, protein, and total energy.

A high-performance gel permeation chromatography fluorescence detection (HPGPC-FD) method combined with fluorescein isothiocyanate (FITC) labeling was established for the microanalysis of L. barbarum polysaccharides (LBP). The calibration curves linear over the range of 0.2–20 µg/mL in rat plasma, and 0.25–500 μg/mL in urine and feces samples with correlation coefficients greater than 0.99. The inter-day and intra-day precisions (RSD, %) of the method were under 15% with the relative recovery ranging from 84.6% to 104.0% and the RSD ranging from 0.47% to 7.28%. The concentration–time curve of LBP-FITC in plasma following intragastric administration at 100, 50 and 25 mg/kg well fitted to a nonlinear model. LBP-FITC slowly eliminated from plasma according to the long half-lives (t1/2 = 31.39, 38.09, and 45.76 h, respectively) and mean retention times (MRT0–t = 18.38, 19.15 and 20.07 h, respectively; AUC0–∞ = 230.49, 236.18 and 242.57 h, respectively) after administration of LBP-FITC at doses of 100, 50, and 25 mg/kg, respectively. After intragastric administration at 50 mg/kg for 72 h, the concentration of LBP-FITC in urine and feces was 0.09 ± 0.04% and 92.18 ± 3.61% respectively; the excretion rate of urine was the highest in 0–4 h period and decreased continuously in 4–24 h period. The excretion rate of feces was the highest in 4–10 h, 48.28 ± 9.349% in feces within 4–10 h, and decreased rapidly in 10–24 h. The present study showed that LBP was absorbed as its prototype and most proportion of LBP was excreted from feces, indicating a long time remaining in intestine.

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Bioactive compounds provide new insights into the prevention and treatment of obesity. Lycium barbarum polysaccharide (LBP), a biological macromolecule extracted from Goji berry, has displayed potential for regulating lipid metabolism. However, the relationship between gut microbiota regulation and lipid metabolism is not entirely clear. In the present study, 50, 100, and 150 mg/kg LBP were intragastrically administered to C57BL/6J male mice fed with a high-fat diet simultaneously lasting for twelve weeks. The results showed that 150 mg/kg LBP showed significant results and all doses of LBP feeding (50, 100, 150 mg/kg) remarkably decreased both serum and liver total cholesterol (TC) and triglyceride (TG) levels. Treatment of 150 mg/kg LBP seems to be more effective in weight loss, lowering free fatty acid (FFA) levels in serum and liver tissues of mice. LBP feeding increased the gene expression of adiponectin and decreased the gene expression of peroxisome proliferator-activated receptor γ, Cluster of Differentiation 36, acetyl-coA carboxylase, and fatty acid synthase in a dose-dependent manner. In addition, the 16s rDNA Sequencing analysis showed that 150 mg/kg LBP feeding may significantly increase the richness of gut microbiota by up-regulation of the ACE and Chao1 index and altered β-diversity among groups. Treatment of 150 mg/kg LBP feeding significantly regulated the microbial distribution by decreasing the relative abundance of Firmicutes and increasing the relative abundance of Bacteroidetes at the phylum level. Furthermore, the relative abundance of Faecalibaculum, Pantoea, and uncultured_bacterium_f_Muribaculaceae at the genus level was significantly affected by LBP feeding. A significant correlation was observed between body weight, TC, TG, FFA and bile acid and phyla at the genus level. The above results indicate that LBP plays a vital role in preventing obesity by co-regulating lipid metabolism and gut microbiota, but its effects vary with the dose.