Volume 10 · Issue 09 · 2018

Nutrition therapy is one of the important components in the comprehensive treatment of diabetes, and the implementation of diabetes management with nutrition therapy can effectively optimize blood sugar control. Glycosylated hemoglobin (HbA) in adult patients with type 1 diabetes and type 2 diabetes can be increased by nutritional therapy_1c) decreased by 1.0% ~1.9%, respectively^[1,2]And 0.3% to 2.0%^[3,4]For children with diabetes, it also helps blood sugar reach the standard^[5,6]。 The nutritional treatment of diabetes in children and adolescents should not only ensure the physiological needs of different growth stages, but also take into account the needs of children's psychological factors, appetite and taste. Since 2000, the International Society for Pediatric and Adolescent Diabetes (ISPAD) first published the clinical practice guidelines for childhood and Adolescent Diabetes. The guidelines cover the content of nutrition management to guide the nutritional treatment of children with Diabetes, and emphasize the importance of nutritional treatment for childhood and Adolescent Diabetes. At present, the concepts and methods of nutrition management of childhood diabetes are different in various regions in China. There is no nutrition treatment guideline or consensus for childhood and adolescent diabetes, and there is an urgent need for a scientific and operable nutrition treatment consensus that can guide clinical practice. Based on the relevant guidelines and consensus of ISPAD, American Diabetes Association (ADA) and Diabetology Branch of Chinese Medical Association (CDS), this article, together with domestic experts and scholars in related fields, and with reference to the latest research results and evidence-based medical evidence at home and abroad, formed the 2018 expert consensus on nutritional treatment of children and adolescents with diabetes, aiming to guide clinicians to carry out standardized nutritional treatment for children with diabetes, so as to help them improve their blood sugar management level and quality of life, promote the research on nutrition of children and adolescents with diabetes, and lay the foundation for further formulating domestic medical nutritional treatment guidelines for children and adolescents with diabetes in the future.

Diabetes is a metabolic disease characterized by hyperglycemia and is the fastest growing disease in the world at present. About 425 million adults worldwide developed diabetes in 2017, and this number will grow to 629 million by 2045^[1]。 The acute and chronic complications caused by diabetes have brought a heavy economic burden to society. Existing therapeutic strategies fail to prevent disease progression and chronic complications from occurring; Due to the existence of metabolic memory, it is of great significance to identify people with high risk of complications early in diagnosis and treatment and formulate personalized treatment plans in time. With the deepening of the understanding of the etiology and prognosis of diabetes, the methods of diabetes classification are also gradually improved. In 1980, WHO classified diabetes into insulin dependent diabetes mellitus (IDDM) and non-insulin dependent diabetes mellitus (NIDDM), and the names are common to type I diabetes and type II diabetes. In 1985, WHO deleted the names of type I and type II diabetes, retained the names of IDDM and NIDDM, and added the types of malnutrition-related diabetes. Until 1999, WHO put forward a unified etiological diabetes classification criteria, namely: type 1 diabetes (T1DM), type 2 diabetes (T2DM), gestational diabetes and special types of diabetes. This classification is still used today, and has been adopted by countries all over the world.

There are many descriptions of the classic special type of diabetes. The most detailed one is the book "Special Types of Diabetes" compiled by Academician Xiang Kunsan^[1]Every time I read it, it will feel timeless. Here I want to talk mainly about the awareness of some atypical manifestations of specific types of diabetes.

A low-carb diet strictly restricts carbohydrates and increases fat intake. Studies in recent decades have shown that low-carb diets can effectively combat obesity and diabetes^[1]。 This article discusses low-carb diet and its therapeutic effect on refractory diabetes, hoping to bring new ideas for clinicians to treat diabetes.

To explore the clinical features, treatment and prognosis of fulminant type 1 diabetes mellitus (FT1DM).

Patients admitted in Peking Union Medical College Hospital from January 2012 to March 2018 with the diagnose of FT1DM were enrolled in the study. All the clinical data were collected and analyzed.

A total of 22 patients were enrolled with 10 males and 12 females. The median age was 31 years old and the median duration of the disease onset was 3 days. Cold-like symptoms and gastrointestinal symptoms with elevated pancreatic enzymes right before the onset were observed in more than half of the patients. Islet-related autoantibodies were negative in 20 patients, while glutamate decarboxylase antibody was positive in 2 patients and 4 patients were found to be positive for autoantibodies other than islet-related autoantibodies. Rubella virus infection was confirmed in 1 case, while FT1DM manifested in 3 cases soon after drug hypersensitivity syndrome (DIHS) and 3 cases happened during pregnancy. All patients were treated with insulin preparations, of which 5 patients manifested as robust blood glucose fluctuations and frequent hypoglycemia at night. Insulin autoantibodies was found to be positive in the above 5 patients, thus the diagnose of EIAS was probable.

FT1DM has remarkably abrupt onset and could be lethal. Lifelong injection of insulin preparations is necessary. When encountered with unexplained blood glucose fluctuations, the possibility of EIAS should be considered.

To elucidate the clinical characteristics and genotype-phenotype relationships of Chinese patients with neonatal diabetes mellitus (NDM) caused by forkhead box P3 (FOXP3) gene mutations (FOXP3-NDM).

A total of 50 suspected patients with NDM were recruited from Peking Union Medical College Hospital. After the detailed collection of clinical information, target sequencing of 21 known causative genes of NDM were performed for molecular genetic diagnosis.

Three patients with FOXP3-NDM were identified, separately carrying FOXP3 p.R312H, p.V408M, and p.P133L hemizygous mutations. All these 3 patients showed simple permanent NDM, without other common manifestations of IPEX syndrome until 9-12 years old. And they only need insulin therapy. However, all the foreign reported cases presented multiple autoimmune diseases besides NDM, and needed immunosuppressive therapy, even with the same mutation.

This is the first report of Chinese FOXP3-NDM patients, which showed totally different clinical phenotypes from foreign reported cases. The underlying molecular mechanism remains to be further studied.

To assess the relationship between serum chemerin, visfatin, ferritin and the risk of gestational diabetes mellitus (GDM).

According to nested case-control study design, a total of 300 pregnant women who took prenatal care in Obstetrics and Gynecology Hospital of Fudan University were chosen as the cohort, clinical information and serum samples during 13 to 17 weeks were collected. A total of 42 women with GDM who were tested by 75 g oral glucose tolerance test (OGTT) during 24 to 28 weeks of pregnancy and 90 age-matched normal women were screened. Serum levels of chemerin, visfatin, ferritin and other indexes were determined. Data were expressed as ±s or median (interquartile interval), and were analyzed using student'st-test, Wilcoxon rank-sum test, one-way ANOVA, Kruskal-Wallis test, Chi-square test, Pearson correlation and Logistic regression accordingly.

(1) Serum concentrations of chemerin [(83±14) vs (74±12) μg/L, t=-3.628, P<0.001] and visfatin [53(88) vs 27(90) μg/L, H=-2.787, P=0.005] were significantly higher than those in the control group. Serum ferritin [65(67) vs 62(53) μg/L, H=-0.269, P=0.788] showed no difference between the two groups. (2) Ferritin was demonstrated unrelated to visftin (r=0.058, P=0.512) and chemerin (r=0.035, P=0.693). There was a positive correlation between chemerin and one hour postprandial plasma glucose (r=0.267, P=0.002) and two hour postprandial plasma glucose (r=0.212, P=0.015). There was a positive correlation between visfatin and OGTT fasting plasma glucose (r=0.180, P=0.039). (3) Chemerin was positively associated with GDM risk even after adjustment for age, body mass index, fasting plasma glucose, homocysteine and high-density lipoprotein-cholesterol, OR (95%CI) were 1.069(1.029-1.112), P=0.001.

Serum concentrations of chemerin and visfatin in early midtrimester are significantly higher in GDM and are irrelevant to ferritin. Elevated levels of chemerin during 13 to 17 weeks of pregnancy is an independent risk factor for GDM.

To explore the interaction between family history of diabetes and abnormal waist-to-height ratio (WHtR) on risk of type 2 diabetes mellitus (T2DM).

The Jinchang cohort (established in June, 2012) was used in this study, and the baseline data were collected in December 2013. For case-control study, 1 109 male patients and 834 female patients with T2DM were included in diabetic group, whereas 1 943 healthy subjects matched with gender were included in control group. The additive model was used to study the interaction; the adjusted OR values of risk factors and regression coefficient were analyzed by multivariate logistic regression analysis; and the interaction between the factors were analyzed by the EXCEL software developed by Andersson et al.

After excluding 26 706 cases without data of waist circumeference, a total of 21 292 cases were included in our study. The prevalence of diabetes was 9.13% (1 943/21 292) in all subjects, but 9.11% (1 109/12 175) in male subjects and 9.15% (834/9 117) in female subjects. After adjusting for age, smoking, drinking and other confounding factors, there was positive additive interaction between family history of diabetes and abnormal WHtR on risk of T2DM. While the family history of diabetes and abnormal WHtR existing at the same time, the risk of diabetes was 9.09 (95%CI: 5.64-14.64) in male and 13.08 (95%CI: 6.99-24.47) in female compared with control. In male, the index of synergistic effect, the attribution of interaction effect, and the percentage of attribution of interaction effect was 1.58, 2.98 and 32.8%, respectively. In female, the index of synergistic effect, the attribution of interaction effect, and the percentage of attribution of interaction effect was 1.90, 5.72 and 43.7%, respectively.

Family history of diabetes and abnormal WHtR may have synergistic effect on risk of T2DM.

To investigate the effects and underlying mechanisms of different doses of liraglutide on the expressions of transforming growth factor-β1 (TGF-β1) and type 1 collagen (Col-1) in myocardial tissue of rats with type 2 diabetes mellitus (T2DM).

A total of 40 healthy male Sprague-Dawley rats aged 4 weeks and weighing (200±20) g were selected and divided into normal control group (group N, 10 rats) and model group (30 rats) according to random number table. Rats in the model group were given high glucose and high fat diet for 8 weeks, and then were injected with 1% streptozotocin into the abdominal cavity in a single dose of 30 mg/kg after molding. Rats in the model group were further divided into three groups: T2DM group (group D, 8 rats), low-dose intervention group (group LD, 7 rats) and high-dose intervention group (group LG, 7 rats). Rats in LD and LG groups were injected with 50 μg/kg or 200 μg/kg liraglutide intraperitoneal twice daily whereas rats in group D were given equal volume of saline. At the end of 8 weeks, all the rats were weighed and anaesthetized to collect blood samples for the tests of blood glucose, blood lipid and other biochemical indexes. The myocardial tissues were collected to study the pathological changes under light microscope after HE staining. The expressions of TGF-β1 and Col-1 were detected by immunohistochemical method, and the expressions of TGF-β1 and Col-1 mRNA were detected by real-time fluorescence quantitative polymerase chain reaction method. Differences among groups were compared by one-way analysis of variance, pairwise comparison was conducted by using LSD- t test.

(1) Compared with group N, the collagen fibers in cardiac myocytes and their interstitium were scattered and arranged in disorder, and the level of TGF-β1 and Col-1 mRNA were increased significantly in group D (0.90±0.23 vs 0.18±0.06, 2.63±1.84 vs 0.52±0.11,t=19.108, 22.779, respectively, all P<0.05). (2) Compared with group D, the degree of myocardial fibrosis and the level of TGF-β1 and Col-1 mRNA in group LD and group LG were decreased (TGF-β1 and Col-1 mRNA in group LD were 0.46±0.13 vs 0.90±0.23, 1.43±0.32 vs 2.63±1.84,t=21.135, 23.548, respectively; those in group LG were 0.29±0.06 vs 0.90±0.23, 0.89±0.12 vs 2.63±1.84, t=18.398, 20.159, respectively, all P<0.05), and the above changes were dose-dependent.

Liraglutide may inhibit fibrosis by down-regulating the expression of TGF-β1 and finally the formation of Col-1. Therefore, liraglutide may possess anti-myocardial fibrosis effect, which may delay the occurrence and development of myocardial lesions in T2DM.

To observe the changes of retinoblastoma (Rb) protein expression in periconceptional mouse pancreatic islet cells and to explore its relationship to β cell proliferation.

6 to 8 weeks, 20-25 g C57BL/6 mice were kept in unpregnancy (NP), 14.5 d and 18.5 d of pregnancy (P14.5, P18.5), 4 d and 8 d after parturition (AP4, AP8) by detecting the vaginal plug. The islets of the mice were isolated and purified by collagenase digestion. The expressions of Rb, phosphorylated Rb (p-Rb) and transcription factor E2F1 were detected by Western blot, and the distributions of Rb and p-Rb were detected by immunofluorescence (IF). Pancreatic-specific Rb knockout (KO) mice were kept in NP, P14.5 and P18.5. Glucose tolerance were assessed by intraperitoneal glucose tolerance test at P18.5. Insulin levels stimulated by glucose were detected in vivo and in vitro. Changes of β cell number, area and size were tested by immunohistochemistry and the Ki67 positive β cells of Rb-KO mice were detected by IF. Differences between groups were compared by independent-sample t test.

(1) During pregnancy, Rb, p-Rb and E2F1 peaked at P14.5, increased 2.16, 2.96 and 2.09 times (t=9.31, 24.23, 8.31, all P<0.01) respectively compared with NP, and returned back gradually after parturition. Rb located mainly in nucleus while p-Rb located in cytoplasm. (2) At NP and P14.5, compared with wild type (WT) mice, Rb-KO mice had better glucose tolerance with less area under the cure (AUC) [(1 343±19) vs (1 511±16) mmol·L^-1·min^-1, t=10.48, P<0.01; (1 073±117) vs (1 359±101) mmol·L^-1·min^-1, t=3.71, P<0.01, respectively]. At P14.5, the insulin levels stimulated by glucose at 2 min and 30 min in Rb-KO mice were significantly higher than those in WT mice [(0.69±0.10) vs (0.55±0.10) ng/ml, (0.46±0.08) vs (0.36±0.08) ng/ml, t=2.40, 2.30, respectively, both P<0.05]. The levels of insulin secretion by glucose stimulation in vitro of KO mice were also higher than those of WT mice in pregnancy [with lower and higher glucose: (233±48) vs (93±49) U/ml, (365±46) vs (230±94)U/ml, t=4.30, 2.62, respectively, both P<0.01]. At NP, the β cell mass, numbers and Ki67 positive β cells increased in Rb-KO mice than those in WT mice ( t=4.53, 3.46, 7.68, all P<0.05), but no significant differences were found in Rb-KO mice between NP and pregnancy.

The expressions of Rb and E2F1 increase during periconception, which are associated with β cell proliferation.

Diabetic foot is a foot ulcer, infection and/or deep tissue destruction associated with distal nerve abnormalities of lower limbs and different degrees of peripheral vascular lesions. It is one of the chronic complications of diabetes mellitus, and it is an important cause of moderate disability, loss of ability and even death in diabetic patients. In recent years, there are few reports of diabetic foot complicated with beriberi. Because of its non-specific clinical and imaging manifestations, it is easy to misdiagnose and misdiagnose. A case of diabetic foot with vitamin B was reported₁The process of diagnosis and treatment is lacking and discussed in conjunction with the literature.

Approximately 360 million people worldwide have varying degrees of hearing impairment. Hearing impairment is one of the common causes of disability, which not only increases patients' medical expenditure, but also affects patients' mental health, social communication and increases non-medical expenditure^[1]。 More than half of congenital and juvenile hearing impairments are due to genetic defects^[2]mitochondrial DNA (mtDNA) defects can lead to hearing impairment in people with different genetic backgrounds^[1,2]。

2002 Kim et al.^[1]Using the ligand-binding domain of the retinoic acid-associated orphan receptor gamma as bait, GLIS (GLI similar, GLIS) 1 was identified using a yeast two-hybrid method. Subsequently, two other members of the GLIS family, GLIS2^[2]and GLIS3^[3]Discovered one after another. The zinc finger domain (ZFD) of GLIS3 has 93% and 59% homology with GLIS1 and GLIS2, respectively; With the exception of ZFD, GLIS3 has low homology with either GLIS1 or any member of the Krüppel-like zinc finger protein family^[3]。