Etiology Of Diabetes Mellitus Research Articles

Effect of honey on postprandial hyperglycemia in alloxan-induced diabetic rats

The role of postprandial hyperglycemia (PPH) is implicated in the etiology of diabetes mellitus and its complications. This study investigated the effect of honey on high glucose-induced PPH in alloxan-induced diabetic rats. Diabetes mellitus was induced by administering alloxan [150 mg/kg body weight (BW)] to overnight fasted rats. The diabetic rats were administered drinking water (1 ml/kg BW) or honey (1, 2 or 3 g/kg BW) via oral gavage. Each group comprised 6 rats. Before administration of drinking water or honey, baseline fasting blood glucose (BG) was measured as BG0. BG levels (BG60, BG120 and BG180) were then measured at 60, 120 and 180 minutes, respectively. Estimation of BG parameters [area under the curve (AUC), peak BG (PBG), percentage (%) variation in BG and % change in BG] was performed. The AUC and PBG did not differ in all the diabetic groups (irrespective of administered agents) compared with diabetic control group. Compared with BG0, the BG60 significantly (p < 0.05) increased in diabetic rats that received drinking water or honey (2 or 3 g/kg BW) but not in diabetic rats that received 1 g/kg BW of honey. The diabetic rats that received 1 g/kg BW of honey exhibited significantly (p < 0.05) lower % change in BG compared with the diabetic control rats. The study showed that administration of honey (irrespective of doses) did not deteriorate high glucose-induced PPH in diabetic rats. The study also indicated that 1 g/kg BW of honey was the most effective dose in suppressing PPH.

Environmental endocrine disruptor-induced mitochondrial dysfunction: a potential mechanism underlying diabetes and its complications.

Diabetes and its complications significantly affect individuals' quality of life. The etiology of diabetes mellitus and its associated complications is complex and not yet fully understood. There is an increasing emphasis on investigating the effects of endocrine disruptors on diabetes, as these substances can impact cellular processes, energy production, and utilization, ultimately leading to disturbances in energy homeostasis. Mitochondria play a crucial role in cellular energy generation, and any impairment in these organelles can increase susceptibility to diabetes. This review examines the most recent epidemiological and pathogenic evidence concerning the link between endocrine disruptors and diabetes, including its complications. The analysis suggests that endocrine disruptor-induced mitochondrial dysfunction-characterized by disruptions in the mitochondrial electron transport chain, dysregulation of calcium ions (Ca2+), overproduction of reactive oxygen species (ROS), and initiation of signaling pathways related to mitochondrial apoptosis-may be key mechanisms connecting endocrine disruptors to the development of diabetes and its complications.

Autophagy and diabetes

The current literature findings on autophagy’s beneficial and detrimental roles in diabetes mellitus (DM) and diabetes-related comorbidities were reviewed. The effects of oral hypoglycaemic medicines and autophagy in DM. Autophagy plays an important function in cellular homeostasis by promoting cell survival or initiating cell death in physiological settings was also assessed. Although autophagy protects insulin-target tissues, organelle failure caused by autophagy malfunction influences DM and other metabolic diseases. Endoplasmic reticulum and oxidative stress enhance autophagy levels, making it easier to regulate stress-induced intracellular changes. Evidence suggests that autophagy-caused cell death can occur when autophagy is overstimulated and constitutively activated, which might prevent or develop DM. Even though the precise role of autophagy in DM complications is uncertain, deregulation of the autophagic machinery is strongly linked to beta cell destruction and the aetiology of DM. Thus, improving autophagy dysfunction is a possible therapeutic objective in treating DM and other metabolic disorders.

Association of MicroRNA-146a with Type 1 and 2 Diabetes and their Related Complications.

Most medical investigations have found a reduced blood level of miR-146a in type 2 diabetes (T2D) patients, suggesting an important role for miR-146a (microRNA-146a) in the etiology of diabetes mellitus (DM) and its consequences. Furthermore, injection of miR-146a mimic has been confirmed to alleviate diabetes mellitus in diabetic animal models. In this line, deregulation of miR-146a expression has been linked to the progression of nephropathy, neuropathy, wound healing, olfactory dysfunction, cardiovascular disorders, and retinopathy in diabetic patients. In this review, besides a comprehensive review of the function of miR-146a in DM, we discussed new findings on type 1 (T1MD) and type 2 (T2DM) diabetes mellitus, highlighting the discrepancies between clinical and preclinical investigations and elucidating the biological pathways regulated through miR-146a in DM-affected tissues.

Comparison of catalase, glutathione peroxidase and malondialdehyde levels in tears among diabetic patients with and without diabetic retinopathy.

Various studies suggest that oxidative stress has a role in the etiology of diabetes mellitus (DM) and its complications. Detection of antioxidant enzymes and malondialdehyde (MDA) level in ocular fluid may provide the possible biomarkers for monitoring the progression of diabetic retinopathy (DR). The aim of this study was to compare catalase, glutathione peroxidase (GPx) and MDA levels in tears among diabetic patients with and without DR. A cross-sectional study was conducted among type 2 DM patients. The patients were divided into three groups: no DR, non-proliferative DR (NPDR) and proliferative DR (PDR). Tears samples were collected using Schirmer strips for measurement of catalase, GPx and MDA. A total of 171 patients were recruited in this study (no DR, 58 patients; NPDR, 57 patients; PDR, 56 patients). There was significant difference in the mean level of GPx in tears between the three groups (no DR, 658.08 ± 115.70 U/L; NPDR, 653.78 ± 87.90 U/L; PDR, 605.31 ± 107.47 U/L, respectively) before and after adjustment for covariates (p = 0.013 and p = 0.001, respectively). Bonferroni post-hoc analysis showed PDR group had significantly lower mean GPx level than in no DR (p=0.001) and NPDR (p=0.037) after adjustment for covariates. There was no significant difference of mean catalase and MDA in the tears between the three groups before and after adjustment for covariates. This study demonstrated that diabetic patient with DR is associated with low level of GPx in tears, suggesting that this antioxidant enzyme is a potential biomarker for predicting the presence of DR.

Characterization of Collapsin Response Mediator Protein 2 in Colorectal Cancer Progression in Subjects with Diabetic Comorbidity.

Background: Common demographic risk factors are identified in colorectal cancer (CRC) and type 2 diabetes mellitus (DM), nevertheless, the molecular link and mechanism for CRC-DM comorbidity remain elusive. Dysregulated glycogen synthase kinase-3 beta under metabolic imbalance is suggested to accelerate CRC pathogenesis/progression via regulating collpasin response mediator protein-2 (CRMP2). Accordingly, roles of CRMP2 in CRC and CRC-DM patients were investigated for elucidating the molecular convergence of CRC and DM. Methods: CRMP2 profile in tumor tissues from CRC and CRC-DM patients was investigated to explore the link between CRC and DM etiology. Meanwhile, molecular mechanism of glucose to regulate CRMP2 profile and CRC characteristics was examined in vitro and in vivo. Results: CRMP2 was significantly lower in tumor lesions and associated with advanced tumor stage in CRC-DM patients. Physiological hyperglycemia suppressed CRMP2 expression/activity and augmented malignant characteristics of CRC cells. Hyperglycemia promotes actin de-polymerization, cytoskeleton flexibility and cell proliferation/metastasis by downregulating CRMP2 profile and thus contributes to CRC disease progression. Conclusions: This study uncovers molecular evidence to substantiate and elucidate the link between CRC and T2DM, as well as characterizing the roles of CRMP2 in CRC-DM. Accordingly, altered metabolic adaptations are promising targets for anti-diabetic and cancer strategies.

Практичне значення діагностики депресії у пацієнтів із цукровим діабетом 2-го типу

Актуальність. Цукровий діабет (ЦД) і депресія сьогодні є поширеними та соціально значущими захворюваннями. Незважаючи на величезну кількість робіт і досліджень, присвячених вивченню причин цих станів, сучасний погляд на етіологію як ЦД, так і депресії залишає безліч нез’ясованих питань. Мета. Продемонструвати практичне застосування шкал діагностики депресії у пацієнтів із ЦД 2-го типу. Матеріали та методи. У дослідження було рандомізовано 190 пацієнтів. Для діагностики депресії використовувалися адаптовані шкали PHQ-9, PAID, WHO, MINI-6, шкала Гамільтона; опрацьовано дані з амбулаторних карт пацієнта за останні 15 років; проведено збір анамнезу, загальний огляд, вимірювання рівня глікованого гемоглобіну та ліпідограми, а також обов’язкову консультацію психіатра, ендокринолога, подолога. Згідно з аналізом зібраних даних і отриманих результатів, пацієнтам призначалися за необхідності седативні препарати, антидепресанти, анксіолітики та психотерапія. Результати. Із загальної кількості пацієнтів (n = 230) після скринінгу було рандомізовано 190 осіб. Стан депресії, виявлений під час інтерв’ю, розцінювався як поточний (протягом двох тижнів) діагноз великого депресивного розладу (Major Depressive Disorder) за Міжнародною класифікацією хвороб 10-го перегляду. Якщо в амбулаторній картці пацієнта епізоди депресії були зафіксовані та задокументовані, то встановлювався діагноз «рекурентна депресія». Обов’язковою також була інформація про стан тривоги та суїцидальні наміри (чи їх спроба в минулому). Після отриманих результатів психіатром приймалося рішення про необхідність прийому седативних препаратів, антидепресантів, анксіолітиків і проведення психотерапії. Висновки. Синергічний ефект тривоги та депресії на стан ЦД підвищує ризик розвитку мікро- та макросудинних ускладнень, спричинює гіперглікемію у пацієнтів та зумовлює пошук нових методів вирішення цієї проблеми.

Evaluation of the Effects of Abdominal Liposuction in Improving Metabolic Parameters in Recently Diagnosed Non Complicated Type 2 Diabetes

Abstract Background: Diabetes Mellitus (DM) is a metabolic disorder characterized by the presence of chronic hyperglyc-emia accompanied by greater or lesser impairment in the metabolism of carbohydrates, lipids and proteins. DM is probably one of the oldest diseases known to man. It was first reported in Egyptian manuscript about 3000 years ago. In 1936, the distinction between type 1 and type 2 DM was clearly made. Type 2 DM was first described as a component of metabolic syndrome in 1988. The origin and etiology of DM can vary greatly but always include defects in either insulin secretion or response or in both at some point in the course of disease. Obesity is associated with an increased risk of premature death and significantly increases the risk of developing type 2 diabetes mellitus, hypertension, coronary heart disease. Dyslipidaemia is a silent pandemic affecting millions of people around the world. There is controversy of the possible benefit of liposuction or abdominoplasty in the metabolism of glucose or cholesterol. Liposuction was the second most frequently performed aesthetic operation in 2013. As with any surgery liposuction carries risks, however, in recent years, improved techniques have made liposuction safer, easier, and less painful. Thus, any intervention that immediately decreases adiposity and is relatively safe could be a viable method not only for aesthetic purpose but also for increasing the efficiency of insulin and improving metabolic profile, especially when combined with regular exercise and proper diet. Aim of Study: The aim of this study is to evaluate the effectiveness of abdominal liposuction in improving quality of life in newly diagnosed uncomplicated type 2 diabetic patients. Patients and Methods: This study will take place in plastic Surgery Department, Port Said general Hospital. As total number of cases satisfying inclusion criteria not exceed 6 cases the study period (During 2019-2020) the total sample 3x6=18 cases all will be included as comprehensive sample. Results: In our study, the mean FBG was 163±22mg/d1 preoperatively. At three months after surgery, it was 162±29mg/dl, but at six months after surgery, it was 147± 28mg/d1. The mean PPBG was 218±40mg/d1 preoperatively. At three months after surgery, it was 216±40mg/dl, but at six months after surgery, it was 200±34mg/d1. The mean HbAlc percentage was 8±0.8% preoperatively. At three months after surgery, it was 7.7±0.8%, but at six months after surgery, it was 7.6±0.8%. The mean triglyceride level 48 preoperatively. At three months after surgery, it was 162±41, but at six months after surgery, it was 159±49. The mean cholesterol was 207 ±42 preoperatively. At three months after surgery, it was 197 ±52, but at six months after surgery, it was 189±41. The HOMA-IR was 3±0.7 preoperatively. At three months after surgery, it was 2.8±0.7, but at six months after surgery, it was 2.8±0.7. All the laboratory investigations change over time among the studied patients were not statistically significant. Conclusion: So, we can conclude that large volume ab-dominal liposuction should not, by itself, be considered a clinical therapy for type 2 diabetes mellitus. Aspiration of large amounts of subcutaneous abdominal fat in diabetic patients, despite having cosmetic benefits, It does not signif-icantly improve insulin sensitivity through altering serum levels of obesity markers. Therefore, the procedure is safe and may could successfully help diabetic subjects to reduce their potential metabolic risks. Therefore, abdominal Liposuc-tion is effective scarless operation for subcutaneous adipose fatty tissue reduction.

Upaya peningkatan kesadaran preventif terhadap diabetes mellitus pada generasi milenial

Diabetes mellitus merupakan salah satu penyakit tidak menular yang menyebabkan gangguan metabolisme. Faktor penyebab diabetes mellitus antara lain keturunan, virus yang menimbulkan kerusakan sel beta pankreas, pola makan, kegemukan, pola aktivitas, lingkungan dan kebiasaan tidur. Kegiatan pengabdian pada masyarakat bertujuan untuk meningkatkan pengetahuan remaja terhadap pencegahan penyakit tidak menular khususnya diabetes melitus. Kegiatan yang dilakukan berupa penyuluhan tentang tanda dan gejala gejala umum dan faktor risiko penyakit tidak menular beserta komplikasinya, pendampingan analisis mandiri kualitas tidur, indeks massa tubuh, pengukuran lingkar lengan atas dan analisis kadar glukosa darah. Hasil dari kegiatan ini, didapatkan peningkatan pengetahuan remaja tentang penyakit tidak menular (khususnya diabetes melitus) serta tentang upaya promotif dan preventif dari penyakit tersebut. Perlu dilakukan kegiatan pengabdian yang berkesinambungan kepada remaja sehingga kesehatan bisa meningkat.

Environmental factors and life style having an impact on pathogenesis and etiology of Diabetes Mellitus

Type 2 diabetes mellitus (T2DM) is currently a public health problem worldwide and a threat to human health and social development. The incidence rate of the disease is steadily increasing. Various genetic and environmental factors have been established as influencing the pathogenesis of this disease. However, the influence of social factors and the natural environment on DM incidence should also be considered. Low-grade inflammation could represent a central point of connection integrating all these potential triggers, being partly responsible for the development of insulin resistance. This paper aims to elaborate on the impact of the natural environment and social factors on DM development, with a special focus on six aspects of the pathogenesis of DM: pollution, radiation, psychology, drink, sleep, and exercise. We identified a two-way relationship between T2DM and social and natural environments. Changes in these environments may lead to low-grade inflammation, which in turn induces or aggravates T2DM and vice versa. Poor lifestyle may lead to increased insulin resistance and promote DM development. Improvements in blood glucose control can be achieved through non-environmental and behavioral interventions.

The role of endocrine disruptors in the etiology of diabetes mellitus.

The role of endocrine disruptors in the etiology of diabetes mellitus.

Effect of dexmedetomidine on ischemia-reperfusion injury of liver and kidney tissues in experimental diabetes and hepatic ischemia-reperfusion injury induced rats

Background: Reperfusion following ischemia can lead to more injuries than ischemia itself especially in diabetic patients. The aim of this study was to evaluate the effect of dexmedetomidine on ischemia-reperfusion injury (IRI) in rats with have hepatic IRI and diabetes mellitus.

Role of C - reactive protein (CRP) as a Marker of an Acute Phase Response in Case Of Diabetes Mellitus: A Mini Review

Diabetes Mellitus is one of the most common major public health problems having worldwide distribution. Depending on the etiology of diabetes mellitus, factors contributing to hyperglycemia may include; reduced insulin secretion, decreased glucose usage and increased glucose production. Recently, there in increasing evidence that an ongoing cytokine induced acute phase response which is sometimes called low grade inflammation, but part of a widespread activation of the innate immune system, is closely involved in the pathogenesis of type 2 diabetes mellitus and associated complications such as dyslipidemia and atherosclerosis. Elevated circulatory inflammatory markers such as C-reactive protein and interleukin-6 predict the development of type 2 Diabetes mellitus and several drugs with anti-inflammatory properties both lower both acute phase reactants and glycemia and possible decrease the risk of developing type 2 diabetes mellitus. In this mini review article, we aimed to systematically review the role of C-reactive protein (CRP) as inflammatory marker with increased risk of type 2 diabetes as well the relation with type 1 diabetes

Heterogeneity in the aetiology of diabetes mellitus in young adults: A prospective study from north India.

Background & objectives:In contrast to Caucasians of European origin, the aetiology of diabetes mellitus (DM) in young adults in other ethnic groups, including Indians is likely to be heterogeneous and difficult to determine. This study was undertaken to determine the aetiology of diabetes in young Indian adults using a protocol-based set of simple clinical and investigation tools.Methods:In this prospective study, 105 Indian young adults with diabetes (age at onset 18-35 yr; duration <2 yr) were studied for a period of 1-3 years. Pancreatic imaging, fasting C-peptide, islet antibodies (against glutamic acid decarboxylase, tyrosine phosphatase and zinc transporter-8) and mitochondrial A3243G mutational analysis were performed in all patients. Four patients were screened for maturity-onset diabetes of the young (MODY) using next-generation sequencing.Results:Type 1 and type 2 diabetes mellitus (T1DM and T2DM) were equally frequent (40% each), followed by fibrocalculous pancreatic diabetes (FCPD, 15%). Less common aetiologies included MODY (2%), mitochondrial diabetes (1%) and Flatbush diabetes (2%). There was considerable phenotypic overlap between the main aetiological subtypes. Elevated islet antibodies were noted in 62 per cent of T1DM patients [positive predictive value (PPV) 84%; negative predictive value (NPV) 78%] while low plasma C-peptide (<250 pmol/l) was present in 56 per cent of T1DM patients [PPV 96% (after excluding FCPD), NPV 72%]. Using these tests and observing the clinical course over one year, a final diagnosis was made in 103 (99%) patients, while the diagnosis at recruitment changed in 23 per cent of patients.Interpretation & conclusions:The aetiology of diabetes in young adults was heterogeneous, with T1DM and T2DM being equally common. FCPD was also frequent, warranting its screening in Indian patients. Testing for islet antibodies and C-peptide in this age group had good PPV for diagnosis of T1DM.

The Relationship between Frequently Used Glucose-Lowering Agents and Gut Microbiota in Type 2 Diabetes Mellitus.

Metabolic diseases, especially diabetes mellitus, have become global health issues. The etiology of diabetes mellitus can be attributed to genetic and/or environmental factors. Current evidence suggests the association of gut microbiota with metabolic diseases. However, the effects of glucose-lowering agents on gut microbiota are poorly understood. Several studies revealed that these agents affect the composition and diversity of gut microbiota and consequently improve glucose metabolism and energy balance. Possible underlying mechanisms include affecting gene expression, lowering levels of inflammatory cytokines, and regulating the production of short-chain fatty acids. In addition, gut microbiota may alleviate adverse effects caused by glucose-lowering agents, and this can be especially beneficial in diabetic patients who experience severe gastrointestinal side effects and have to discontinue these agents. In conclusion, gut microbiota may provide a novel viewpoint for the treatment of patients with diabetes mellitus.

Aetiology of Diabetes Mellitus and Implications from a Prospective Single Centre Study in Chinese Patients

Aetiology of Diabetes Mellitus and Implications from a Prospective Single Centre Study in Chinese Patients

Diabetogenic Effects of Ochratoxin A in Female Rats.

In this study, the diabetogenic effects of long term Ochratoxin A (OTA) administration in rats were investigated, and its role in the etiology of diabetes mellitus (DM) was examined utilizing 42 female Wistar rats for these purposes. The rats were divided into three different study and control groups according to the duration of the OTA administration. The rats received 45 μg OTA daily in their feed for 6, 9 and 24 weeks, respectively. Three control groups were also used for the same time periods. Blood and pancreatic tissue samples were collected during the necropsy at the end of the 6, 9 and 24 weeks. The plasma values of insulin, glucagon and glucose were determined for the study and control groups. Pancreatic lesions were evaluated via histopathological examination and insulin and glucagon expression in these lesions was subsequently determined using immunohistochemical methods. Statistically significant decreases in insulin levels were observed, in contrast to increases in blood glucagon and glucose levels. Histopathological examinations revealed slight to moderate degeneration in Langerhans islet cells in all OTA-treated groups. Immunohistochemistry of pancreatic tissue revealed decreased insulin and increased glucagon expression. This study demonstrated that OTA may cause pancreatic damage in the Langerhans islet and predispose rats to DM.

Role of Serum Adiponectin and Vitamin D in Prediabetes and Diabetes Mellitus.

The roles of deficient or deranged insulin, adiponectin and 25 hydroxy vitamin D (25[OH]D) levels regulating food intake, energy metabolism, glucose and lipid metabolism and body weight have been reported in the pathogenesis of prediabetes and type 2 diabetes mellitus. However, their congruity in the etiology of diabetes mellitus is unknown. Thus, the aim of the study was to investigate the roles of these parameters together and to establish their interrelationship in patients with prediabetes and diabetes. The preliminary cross-sectional study included 77 persons with type 2 diabetes who were matched for age, sex and body mass index (BMI); 73 persons with prediabetes; and 52 healthy control subjects. Fasting serum levels of adiponectin, insulin and 25(OH)D were measured by commercially available immune assay kits, and routine biochemical parameters were analyzed in all study groups. The results show statistically significant lower levels of serum adiponectin and serum 25(OH)D and higher serum insulin levels in persons with prediabetes or type 2 diabetes with respect to controls. The changes in the serum adiponectin or serum 25(OH)D in persons with prediabetes and type 2 diabetes were found to be inversely correlated with the serum levels of insulin. Moreover, multiple linear regression analysis, with 25(OH)D, insulin and homeostatic model assessment-insulin resistance (HOMA-IR) as the variables, revealed that serum adiponectin levels might be an independent risk factor for the progression of prediabetes and type 2 diabetes in subjects. The association of these hormones might act as a significant predictor of progression of prediabetes to type 2 diabetes. Decreased serum adiponectin levels might be an independent risk factor for progression to prediabetes and type 2 diabetes, which may help in developing experimental models of the disease or in identifying biomarkers or disease-modifying drugs.

Diabetes: Controlling the identity of the adult pancreatic β cell.

Understanding how pancreatic β cells achieve and maintain functional identity as insulin-secreting cells is a major roadblock in our understanding of the aetiology of diabetes mellitus. Three new papers reveal the roles, in the adult β cell, of four transcription factors that are crucial for reprogramming a multipotent endocrine progenitor.

Gut microbiota and immunopathogenesis of diabetes mellitus type 1 and 2.

Diabetes mellitus (DM) is a major increasing global health burden in the aging population. Understanding the etiology of DM is beneficial for its prevention as well as treatment. In light of the metagenome hypothesis, defined as the overall bacterial genome, gut microbes have attracted increasing attention in the pathogenesis of DM. Many studies have found that gut microbes are involved in the immunopathogenesis of DM. Probiotics strengthen the host's intestinal barrier and modulate the immune system, and have therefore been investigated in DM management. Recent epigenetic findings in context of genes associated with inflammation suggest a possible way in which gut microbiota participate in the immunopathogenesis of DM. In this review, we discuss the role of gut microbiota in the immunopathogenesis of DM.