Effects of resistant dextrin on liver fat deposition and the AMPK signaling pathway in high-fat diet-fed mice / 中华内分泌代谢杂志

Objective@#To study the effects of resistant dextrin (RD) on liver fat deposition in high-fat diet-fed (HFD) mice, and to further explore whether it can regulate the AMPK signaling pathway.@*Methods@#Thirty-six 4-week-old male C57BL/6 mice were randomly divided into three groups: normal control group (chow), high-fat diet group (HFD), and high-fat diet+ resistant dextrin group (HFD+ RD, 10 g·kg-1·d-1). After 12 weeks of intervention, the liver tissues and serum samples were collected. Serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), aspartate aminotransferase (AST), alanine transaminase (ALT) levels and liver TG were measured. Liver tissue HE and oil red O staining were performed to observe hepatocyte steatosis and liver fat deposition. Quantitative real-time PCR was performed to detect the relative expression of fatty acid synthesis related genes SREBP1, ACC, SCD1 in the liver tissue, and Western blot was performed to detect relative protein levels of pAMPK, SREBP1, Fasn, and ACC in the liver.@*Results@#Compared with chow group, the body weight gain, fasting blood glucose (FBG), serum TC, LDL-C, HDL-C, and ALT levels were increased in HFD group (P<0.01), and serum AST level was also increased (P<0.05). Moreover, liver oil red O staining revealed that liver fat deposition was much more obvious in HFD group than that in chow group, and liver TG was also increased in HFD group (P<0.01). The mRNA levels of SREBP1 and ACC were increased in HFD group compared with that in chow group, and the protein level of pAMPK was reduced in HFD group (P<0.05). As compared with HFD group, the body weight gain, serum TG, TC, LDL-C, HDL-C and ALT levels were significantly reduced in RD group (P<0.01), and FBG level was also reduced (P<0.05). Moreover, RD treatment alleviated liver fat deposition and TG accumulation (P<0.01). The mRNA levels of SREBP1, ACC, and SCD1 were all reduced in RD group compared with HFD group. The protein level of pAMPK was increased, and the expression of Fasn was reduced with RD treatment (P<0.01).@*Conclusion@#Resistant dextrin improves liver fat deposition and activates the AMPK signaling pathway in HFD-fed mice.

Correlation between serum dipeptidyl peptidase 4 activity and abnormal lipid metabolism / 中华内分泌代谢杂志

Objective:Dipeptidyl peptidase 4 (DPP4) is an incretin lyase, while DPP4 inhibitors have been used clinically as hypoglycemic drugs. Serum DPP4 is related to metabolic diseases such as cardiovascular disease and obesity, and lipid metabolic disorder is an important part of metabolic syndrome. This study was designed to explore the relationship between DPP4 and lipid metabolic disorder.Methods:There were 3644 participants from Chengqiao Town, Chongming District, Shanghai. All of the subjects recruited were residents between 40-70 years old, who have not diagnosed as diabetes mellitus (DM) and who have never used any lipid-lowering drugs. Glucose, insulin, lipid level, DPP4 activity and liver enzymes in serum of all participants were tested. In addition, height, weight and blood pressure were also recorded.Results:Participants were divided into four groups (Q1-Q4) according to the quartile value of serum DPP4 activities. Along with the increase of serum DPP4 activity, triglyceride, total cholesterol, and blood glucose levels increased, and triglyceride increased from (1.23 ± 0.70) mmol/L to (2.31 ± 1.89) mmol/L. Compared with cholesterol levels, the triglyceride was more closely related to DPP4 activity [the correlation coefficients of triglyceride, total cholesterol, low-density lipoprotein-cholesterol (LDL-C), and high-density lipoprotein-cholesterol (HDL-C) were 0.424, 0.281, 0.142, and 0.027, respectively]. After adjusting for confounding factors (age, gender, BMI), the result was similar. With the increase of DPP4 enzyme activity, the Q4 group had a higher risk of developing hyperglyceridemia ( OR=5.25) than the Q1 group, and the result was almost unchanged after adjusting for confounding factors and blood glucose levels ( OR=4.90). Conclusion:Serum DPP4 activity is independently related to blood lipid levels, and is particularly closely related to blood TG levels.

Effects of resistant dextrin on liver fat deposition and the AMPK signaling pathway in high-fat diet-fed mice / 中华内分泌代谢杂志

Objective:To study the effects of resistant dextrin (RD) on liver fat deposition in high-fat diet-fed (HFD) mice, and to further explore whether it can regulate the AMPK signaling pathway.Methods:Thirty-six 4-week-old male C57BL/6 mice were randomly divided into three groups: normal control group (chow), high-fat diet group (HFD), and high-fat diet+ resistant dextrin group (HFD+ RD, 10 g·kg -1·d -1). After 12 weeks of intervention, the liver tissues and serum samples were collected. Serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), aspartate aminotransferase (AST), alanine transaminase (ALT) levels and liver TG were measured. Liver tissue HE and oil red O staining were performed to observe hepatocyte steatosis and liver fat deposition. Quantitative real-time PCR was performed to detect the relative expression of fatty acid synthesis related genes SREBP1, ACC, SCD1 in the liver tissue, and Western blot was performed to detect relative protein levels of pAMPK, SREBP1, Fasn, and ACC in the liver. Results:Compared with chow group, the body weight gain, fasting blood glucose (FBG), serum TC, LDL-C, HDL-C, and ALT levels were increased in HFD group ( P<0.01), and serum AST level was also increased ( P<0.05). Moreover, liver oil red O staining revealed that liver fat deposition was much more obvious in HFD group than that in chow group, and liver TG was also increased in HFD group ( P<0.01). The mRNA levels of SREBP1 and ACC were increased in HFD group compared with that in chow group, and the protein level of pAMPK was reduced in HFD group ( P<0.05). As compared with HFD group, the body weight gain, serum TG, TC, LDL-C, HDL-C and ALT levels were significantly reduced in RD group ( P<0.01), and FBG level was also reduced ( P<0.05). Moreover, RD treatment alleviated liver fat deposition and TG accumulation ( P<0.01). The mRNA levels of SREBP1, ACC, and SCD1 were all reduced in RD group compared with HFD group. The protein level of pAMPK was increased, and the expression of Fasn was reduced with RD treatment ( P<0.01). Conclusion:Resistant dextrin improves liver fat deposition and activates the AMPK signaling pathway in HFD-fed mice.

Approach to the patient with vitamin D-deficient osteomalacia due to X-linked agammaglobulinemia / 中华内分泌代谢杂志

Osteomalacia is a metabolic bone disease characterized by impaired mineralization of bone matrix. VitaminD deficiency contributes to a decrease in the efficiency of intestinal calcium and phosphorus absorption, resulting in secondary hyperparathyroidism and an inadequate calcium-phosphorus product, thereby causing osteomalacia. We present a patient who was diagnosed as vitamin D-deficient osteomalacia due to X-linked agammaglobulinemia ( XLA) , and the genetic analysis of the BTK gene revealed a missense mutation ( c.82C>T) . It should be attached great importance to etiological analysis of osteomalacia, and XLA may also be a cause of vitamin D deficiency.

Approach to the patient with hypokalemia caused by Hashimoto′s thyroiditis associated with primary Sjogren′s syndrome and renal tubular acidosis / 中华内分泌代谢杂志

Hypokalemia is a common clinical symptom. It is quite important to clarify the cause of hypokalemia. Autoimmune thyroid disease and primary Sjogren syndrome ( pSS ) have a common genetic predisposition. The coexistence of both diseases is frequent. Renal tubular acidosis ( RTA) is one of the causes of hypokalemia, which can be primary and secondary to other diseases in etiology. Primary RTA is more common in children. As for adults, RTA is often secondary to pSS. In this paper, we reported a case of hypokalemia caused by Hashimoto’s thyroiditis associated with primary Sjogren’s syndrome and renal tubular acidosis in order to call attention to the special cause and treatment of hypokalemia.