Search for other papers by Xiaobing Lu in
Google Scholar
PubMed
Search for other papers by Jiang Yue in
Google Scholar
PubMed
Search for other papers by Qianjing Liu in
Google Scholar
PubMed
Search for other papers by Shengyun He in
Google Scholar
PubMed
Search for other papers by Ying Dong in
Google Scholar
PubMed
Search for other papers by Ming Zhang in
Google Scholar
PubMed
Search for other papers by Yicheng Qi in
Google Scholar
PubMed
Search for other papers by Minglan Yang in
Google Scholar
PubMed
Search for other papers by Wang Zhang in
Google Scholar
PubMed
Search for other papers by Hua Xu in
Google Scholar
PubMed
Search for other papers by Qing Lu in
Google Scholar
PubMed
Search for other papers by Jing Ma in
Google Scholar
PubMed
Background
The aim of this study was to address the intramuscular adipose tissue (IMAT) accumulation in the lower extremities and further detect the relationship between adipose tissue (AT) distribution in the muscle and glucose metabolism in subjects with obesity.
Methods
We conducted a cross-sectional study in 120 Chinese obese adults (80 male and 40 female) with BMI ≥ 28 kg/m2. MRI was applied to access the IMAT content in lower extremities. The oral glucose tolerance test was used to evaluate the glucose metabolism and insulin secretion in all individuals. The correlations between glucose metabolism and the fat content of the lower extremities were further assessed.
Results
Among 120 included subjects, 54 were classified as subjects with normal glucose tolerance (NGT) and 66 with impaired glucose regulation (IGR). We presented that those with IGR had higher fat accumulation in semitendinosus, adductor magnus, gracilis and sartorius than those with NGT (all P < 0.05). In sex-specific analyses, females have higher IMAT in adductor magnus than males (P < 0.001). Males with IGR had higher fat fraction of semitendinosus and sartorius than those with NGT (P = 0.020, P = 0.014, respectively). Logistic regression analyses revealed that IMAT content in semitendinosus was the independent factor of IGR in individuals with obesity after adjustment for age, gender, triglycerides, creatinine and albumin (odds ratio: 1.13, 95% CI: 1.02–1.26, P = 0.024).
Conclusions
Increased adipose tissue accumulation in thigh muscles was associated with glucose dysregulation in patients with obesity. IMAT content in semitendinosus may serve as a possible risk factor for impaired glucose metabolism.
Search for other papers by Tsung-Hui Wu in
Google Scholar
PubMed
Search for other papers by Guan-Yu Su in
Google Scholar
PubMed
Search for other papers by Tsung-Yun Liu in
Google Scholar
PubMed
Institute of Pharmacology, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
PhD Program in Toxicology, Kaohsiung Medical University, Kaohsiung, Taiwan
Search for other papers by Hsiang-Tsui Wang in
Google Scholar
PubMed
Faculty of Medicine, National Yang Ming Chiao Tung University School of Medicine, Taipei, Taiwan
Search for other papers by Chii-Min Hwu in
Google Scholar
PubMed
Acrolein, an unsaturated aldehyde, plays a pathological role in neurodegenerative diseases. However, less is known about its effects on peripheral neuropathy. The aim of this study was to investigate the association of acrolein and diabetic peripheral neuropathy in patients with type 2 diabetes. We recruited 148 ambulatory patients with type 2 diabetes. Each participant underwent an assessment of the Michigan Neuropathy Screening Instrument Physical Examination. Diabetic peripheral neuropathy was defined as Michigan Neuropathy Screening Instrument Physical Examination score ≥ 2.5. Serum levels and urinary levels of acrolein protein conjugates were measured. Urinary acrolein protein conjugates-to-creatinine ratios were determined. Patients with diabetic peripheral neuropathy had significantly higher urinary acrolein protein conjugates-to-creatinine ratios than those without diabetic peripheral neuropathy (7.91, 95% CI: 5.96–10.50 vs 5.31, 95% CI: 4.21–6.68, P = 0.029). Logarithmic transformation of urinary acrolein protein conjugates-to-creatinine ratios was positively associated with diabetic peripheral neuropathy in univariate logistic analysis, and the association remained significant in multivariate analysis (OR = 2.45, 95% CI: 1.12–5.34, P = 0.025). In conclusion, urinary acrolein protein conjugates-to-creatinine ratio may act as a new biomarker for diabetic peripheral neuropathy in type 2 diabetes. The involvement of acrolein in the pathogenesis of diabetic peripheral neuropathy warrants further investigation.
Search for other papers by Henry Zelada in
Google Scholar
PubMed
Search for other papers by M Citlalli Perez-Guzman in
Google Scholar
PubMed
Search for other papers by Daniel R Chernavvsky in
Google Scholar
PubMed
Search for other papers by Rodolfo J Galindo in
Google Scholar
PubMed
Over the last few years, several exciting changes in continuous glucose monitoring (CGM) technology have expanded its use and made CGM the standard of care for patients with type 1 and type 2 diabetes using insulin therapy. Consequently, hospitals started to notice increased use of these devices in their hospitalized patients. Furthermore during the coronavirus disease 2019 (COVID) pandemic, there was a critical need for innovative approaches to glycemic monitoring, and several hospitals started to implement CGM protocols in their daily practice. Subsequently, a plethora of studies have demonstrated the efficacy and safety of CGM use in the hospital, leading to clinical practice guideline recommendations. Several studies have also suggested that CGM has the potential to become the standard of care for some hospitalized patients, overcoming the limitations of current capillary glucose testing. Albeit, there is a need for more studies and particularly regulatory approval. In this review, we provide a historical overview of the evolution of glycemic monitoring in the hospital and review the current evidence, implementation protocols, and guidance for the use of CGM in hospitalized patients.
Department of Endocrinology, Austin Health, Melbourne, Australia
Division of Endocrinology, Diabetes and Metabolism, Northwell, Great Neck, New York, USA
Search for other papers by Yee-Ming M Cheung in
Google Scholar
PubMed
Search for other papers by Rudolf Hoermann in
Google Scholar
PubMed
Search for other papers by Karen Van in
Google Scholar
PubMed
Search for other papers by Damian Wu in
Google Scholar
PubMed
Search for other papers by Jenny Healy in
Google Scholar
PubMed
Search for other papers by Bella Halim in
Google Scholar
PubMed
Search for other papers by Manjri Raval in
Google Scholar
PubMed
Search for other papers by Maria McGill in
Google Scholar
PubMed
Department of Cardiology, Austin Health, Melbourne Australia
Search for other papers by Ali Al-Fiadh in
Google Scholar
PubMed
Search for other papers by Michael Chao in
Google Scholar
PubMed
Search for other papers by Shane White in
Google Scholar
PubMed
Olivia Newton-John Cancer Research Institute, Austin Health, Melbourne, Australia
Search for other papers by Belinda Yeo in
Google Scholar
PubMed
Department of Endocrinology, Austin Health, Melbourne, Australia
Search for other papers by Jeffrey D Zajac in
Google Scholar
PubMed
Department of Endocrinology, Austin Health, Melbourne, Australia
Search for other papers by Mathis Grossmann in
Google Scholar
PubMed
Purpose
We previously demonstrated that 12 months of aromatase inhibitor (AI) treatment was not associated with a difference in body composition or other markers of cardiometabolic health when compared to controls. Here we report on the pre-planned extension of the study. The pre-specified primary hypothesis was that AI therapy for 24 months would lead to increased visceral adipose tissue (VAT) area when compared to controls.
Methods
We completed a 12-month extension to our prospective 12-month cohort study of 52 women commencing AI treatment (median age 64.5 years) and 52 women with breast pathology not requiring endocrine therapy (63.5 years). Our primary outcome of interest was VAT area. Secondary and exploratory outcomes included other measures of body composition, hepatic steatosis, measures of atherosclerosis and vascular reactivity. Using mixed models and the addition of a fourth time point, we increased the number of study observations by 79 and were able to rigorously determine the treatment effect.
Results
Among study completers (AI = 39, controls = 40), VAT area was comparable between groups over 24 months, the mean-adjusted difference was −1.54 cm2 (95% CI: −14.9; 11.9, P = 0.79). Both groups demonstrated parallel and continuous increases in VAT area over the observation period that did not diverge or change between groups. No statistically significant difference in our secondary and exploratory outcomes was observed between groups.
Conclusions
While these findings provide reassurance that short-to-medium-term exposure to AI therapy is not associated with metabolically adverse changes when compared to controls, risk evolution should be less focussed on the AI-associated effect and more on the general development of cardiovascular risk over time.
Search for other papers by Molly L Tanenbaum in
Google Scholar
PubMed
Search for other papers by Persis V Commissariat in
Google Scholar
PubMed
Diabetes technology continues to advance, with more individuals with type 1 diabetes (T1D) adopting insulin pumps, continuous glucose monitoring (CGM), and automated insulin delivery (AID) systems that integrate real-time glucose data with an algorithm to assist with insulin dosing decisions. These technologies are linked with benefits to glycemic outcomes (e.g. increased time in target range), diabetes management behaviors, and quality of life. However, current devices and systems are not without barriers and hassles for the user. The intent of this review is to describe the personal challenges and reactions that users experience when interacting with current diabetes technologies, which can affect their acceptance and motivation to engage with their devices. This review will discuss user experiences and strategies to address three main areas: (i) the emotional burden of utilizing a wearable device; (ii) the perceived and experienced negative social consequences of device use; and (iii) the practical challenges of wearing devices.
Search for other papers by Yang Yu in
Google Scholar
PubMed
Search for other papers by Hairong Hao in
Google Scholar
PubMed
Search for other papers by Linghui Kong in
Google Scholar
PubMed
Search for other papers by Jie Zhang in
Google Scholar
PubMed
Search for other papers by Feng Bai in
Google Scholar
PubMed
Search for other papers by Fei Guo in
Google Scholar
PubMed
Search for other papers by Pan Wei in
Google Scholar
PubMed
Search for other papers by Rui Chen in
Google Scholar
PubMed
Search for other papers by Wen Hu in
Google Scholar
PubMed
Previous studies have shown that the elevated levels of circulating branched-chain amino acids (BCAAs) are associated with the development of insulin resistance and its complications, including obesity, type 2 diabetes, cardiovascular disease and some cancers. However, animal models that can mimic the metabolic state of chronically elevated BCAAs in humans are rare. Therefore, the aim of this study was to establish the above animal model and analyse the metabolic changes associated with high BCAA levels. Sixteen 8-week-old Sprague–Dawley (SD) rats were randomly divided into two groups and given either a high fructose diet or a normal diet. BCAA levels as well as blood glucose and lipid levels were measured at different time points of feeding. The mRNA expression levels of two key enzymes of BCAA catabolism, ACAD (acyl-CoA dehydrogenase) and BCKDH (branched-chain α-keto acid dehydrogenase), were measured by qPCR, and the protein expression levels of these two enzymes were analysed by immunohistochemistry. Finally, the metabolite expression differences between the two groups were analysed by Q300 metabolomics technology. Our study confirms that defects in the catabolic pathways of BCAAs lead to increased levels of circulating BCAAs, resulting in disorders of glucose and lipid metabolism characterized by insulin resistance by affecting metabolic pathways associated with amino acids and bile acids.
Search for other papers by Shaomin Shi in
Google Scholar
PubMed
Search for other papers by Xinghua Chen in
Google Scholar
PubMed
Search for other papers by Wen Yu in
Google Scholar
PubMed
Search for other papers by Xiaolan Ke in
Google Scholar
PubMed
Search for other papers by Tean Ma in
Google Scholar
PubMed
Protection of podocytes is one of the important means to delay the progression of diabetic nephropathy (DN), and glucagon-like peptide-1 (GLP-1) has been shown to have a protective effect on the kidney in DN models, but whether it has a protective effect on podocytes and the potential mechanisms of action remain largely unknown. In the present study, we established a type 2 diabetes mellitus (T2DM) mouse model by high-fat diet feeding combined with streptozotocin (STZ) induction and administered the intervention for 14 weeks. We found that liraglutide significantly ameliorated podocyte injury in DN mice. Mechanistically, we detected glucagon-like peptide-1 receptor (GLP-1R) protein expression levels in kidney tissues by immunohistochemical staining, immunofluorescence staining, and western blotting and found that podocytes could express GLP-1R and liraglutide treatment could restore GLP-1R expression in the kidney tissues of DN mice. Furthermore, we found that NLRP3-induced inflammation and pyroptosis were positively correlated with podocyte injury in DN mice, and liraglutide inhibited the expression of NLRP3-induced inflammation and pyroptosis-related proteins. Our results suggest that liraglutide protects DN mouse podocytes by regulating GLP-1R in renal tissues and by regulating NLRP3-induced inflammation and pyroptosis.
Search for other papers by Zhaoxiang Liu in
Google Scholar
PubMed
Search for other papers by Mingqiang Zhang in
Google Scholar
PubMed
Search for other papers by Xiaohu Shi in
Google Scholar
PubMed
Search for other papers by Wenhui Zhao in
Google Scholar
PubMed
Search for other papers by Chenxiang Cao in
Google Scholar
PubMed
Search for other papers by Lixia Jin in
Google Scholar
PubMed
Search for other papers by Yanlei Wang in
Google Scholar
PubMed
Search for other papers by Jianzhong Xiao in
Google Scholar
PubMed
Objectives
The activation of immune cells plays a significant role in the progression of type 2 diabetes. This study aimed to investigate the potential role of myeloid-derived suppressor cells (MDSCs) and T-regulatory cells (Tregs) in type 2 diabetes.
Methods
A total of 61 patients diagnosed with type 2 diabetes were recruited. Clinical characteristics were reviewed and peripheral blood samples were collected. We calculated the percentage of different cells. Frequencies of MDSC subsets refered to the percentage of G-MDSCs (CD15+CD33+CD11b+CD14-HLA-DR-/low) in CD45 positive cells and the percentage of M-MDSCs (CD14+CD15-CD11b+CD33+HLA-DR-/low) in lymphocytes plus monocytes.
Results
Frequencies of programmed cell death ligand 1-positive granulocytic MDSCs (PD-L1+ G-MDSCs), programmed cell death ligand 2-positive monocytic MDSCs (PD-L2+ M-MDSCs), PD-L2+ G-MDSC, and programmed cell death protein 1-positive Tregs (PD-1+Tregs) were decreased in patients with type 2 diabetes. The frequency of PD-1+ Tregs was positively related to PD-L2+ M-MDSCs (r= 0.357, P = 0.009) and negatively related to HbA1c (r = -0.265, P = 0.042), fasting insulin level (r = −0.260, P = 0.047), and waist circumference (r = −0.373, P = 0.005).
Conclusions
Decreased PD-L2+ M-MDSCs and PD-1+ Tregs may promote effector T cell activation, leading to chronic low-grade inflammation in type 2 diabetes. These findings highlight the contribution of MDSCs and Tregs to the immunopathogenesis of type 2 diabetes and suggest their potential as targets for new therapeutic approaches.
Search for other papers by Ying Pei in
Google Scholar
PubMed
Search for other papers by Rui Wang in
Google Scholar
PubMed
Search for other papers by Wanyu Chen in
Google Scholar
PubMed
Search for other papers by Shulin Yi in
Google Scholar
PubMed
Search for other papers by Chen Huang in
Google Scholar
PubMed
Search for other papers by Shaochan Liang in
Google Scholar
PubMed
Search for other papers by Hongying Cao in
Google Scholar
PubMed
Search for other papers by Yifei Xu in
Google Scholar
PubMed
Search for other papers by Bo Tan in
Google Scholar
PubMed
Background
Similar to the high-fat diet (HFD), the high-glycemic diet (HGD) contributes to the development and progression of type 2 diabetes mellitus (T2DM). However, the effect of HGD on gastrointestinal motility in T2DM and its underlying mechanisms remain unclear.
Methods
Thirty C57BL/6J mice were randomly designated into the normal-feeding diet (NFD) group, HFD group, and HGD group. The plasma glucose, plasma insulin, and gastrointestinal motility were examined. Meanwhile, the tension of isolated colonic smooth muscle rings was calculated, and the gut microbiota was analyzed by 16s rDNA high-throughput sequencing.
Result
After 16 weeks of HGD feeding, obesity, hyperglycemia, insulin resistance, and constipation were observed in HGD mice. Autonomic contraction frequency of the colonic neuromuscular system and electrical field stimulation-induced contractions were reduced in HGD mice. On the contrary, neuronal nitric oxide synthase activity and neuromuscular relaxation were found to be enhanced. Finally, gut microbiota analysis revealed that Rhodospirillaceae abundance significantly increased at the family level in HGD mice. At the genus level, the abundance of Insolitispirillum increased remarkably, whereas Turicibacter abundance decreased significantly in HGD mice.
Conclusion
HGD induced constipation in obese diabetic mice, which we speculated that it may be related to neuromuscular dysmotility and intestinal microbiota dysbiosis.
Search for other papers by Laura Hasse in
Google Scholar
PubMed
Search for other papers by Dagmar Jamiolkowski in
Google Scholar
PubMed
Search for other papers by Felix Reschke in
Google Scholar
PubMed
Search for other papers by Kerstin Kapitzke in
Google Scholar
PubMed
Search for other papers by Jantje Weiskorn in
Google Scholar
PubMed
Search for other papers by Olga Kordonouri in
Google Scholar
PubMed
Search for other papers by Torben Biester in
Google Scholar
PubMed
Search for other papers by Hagen Ott in
Google Scholar
PubMed
Objective
Little is known about specific cutaneous findings in children and adolescents with overweight and obesity. This study assessed the association of skin signs with pivotal auxological and endocrinological parameters and their influence on the quality of life (QoL) of young people with obesity.
Study design
All patients initially recruited for a tertiary hospital's weight control program were offered participation in this interdisciplinary, single-center, cross-sectional study. All participants underwent a detailed dermatological examination, anthropometric measurements and laboratory examinations. QoL was assessed with validated questionnaires.
Results
A total of 103 children and adolescents (age 11.6 ±2.5 years, 41% female, 25% prepubertal, BMI SDS 2.6 ± 0.5, homeostatic model assessment (HOMA) score 3.3 ± 4.2; mean ± s.d.) were recruited in a 12-month study period. Skin affections were linearly associated with increasing BMI and higher age. The most common skin findings were (%) striae distensae (71.0), keratosis pilaris (64.7), acanthosis nigricans (45.0), acne vulgaris (39.2), acrochordons (25.5) and plantar hyperkeratosis (17.6). The HOMA score was associated with acanthosis nigricans (P = 0.047), keratosis pilaris (P = 0.019) and acne vulgaris (P < 0.001). The general mean QoL(QoL) score, as assessed by the WHO-5, was 70 out of 100. A total of 38.9% of participants reported impaired dermatological QoL.
Conclusions
This study shows the high prevalence of skin lesions in children and adolescents with obesity. The association between skin lesions and the HOMA score indicates that skin manifestations are a marker of insulin resistance. To prevent secondary diseases and improve QoL, thorough skin examinations and interdisciplinary cooperation are necessary.
