Cells In Islets Of Langerhans Research Articles

Structural and biochemical analysis of highly similar HLA-B allotypes differentially associated with type 1 diabetes

Type 1 diabetes (T1D) is an autoimmune disease involving T cell-mediated destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans. CD8+ T cells, responding to beta cell peptides presented by class I major histocompatibility complex (MHC) molecules, are important effectors leading to beta cell elimination. Human leukocyte antigen (HLA) B∗39:06, B∗39:01, and B∗38:01 are closely related class I MHC allotypes that nonetheless show differential association with T1D. HLA-B∗39:06 is the most predisposing of all HLA class I molecules and is associated with early age at disease onset. B∗39:01 is also associated with susceptibility to T1D, but to a lesser extent, though differing from B∗39:06 by only two amino acids. HLA-B∗38:01, in contrast, is associated with protection from the disease. Upon identifying a peptide that binds to both HLA-B∗39:06 and B∗39:01, we determined the respective X-ray structures of the two allotypes presenting this peptide to 1.7Å resolution. The peptide residues available for T cell receptor contact and those serving as anchors were identified. Analysis of the F pocket of HLA-B∗39:06 and B∗39:01 provided an explanation for the distinct peptide C terminus preferences of the two allotypes. Structure-based modeling of the protective HLA-B∗38:01 suggested a potential reason for its peptide preferences and its reduced propensity to present 8-mer peptides compared to B∗39:06. Notably, the three allotypes showed differential binding to peptides derived from beta cell autoantigens. Taken together, our findings should facilitate identification of disease-relevant candidate T cell epitopes and structure-guided therapeutics to interfere with peptide binding.

β-Cell Heterogeneity and Plasticity.

The existence of functionally diverse and plastic β cells in islets of Langerhans has been reported since the 1980s. Recently, high-resolution technologies have advanced our understanding of β-cell heterogeneity and plasticity. Here, we define plasticity broadly as dynamic changes in cellular phenotypes and heterogeneity as differences in cellular behaviors. Individual β cells react differently to environmental challenges and act together to maintain β-cell mass and glucose homeostasis within a narrow range of 70-140mg/dL. During the progress of diabetes, this elaborate balance is disrupted, and a lack of β-cell compensation leads to dysregulated blood glucose. In this chapter, we assess β-cell stress that instigates increased β-cell heterogeneity and adaptive β-cell responses such as proliferation, dedifferentiation, maturity, and insulin secretion. We also discuss the maturity, electrical activity, and insulin secretion of well-characterized β-cell subgroups. Finally, we touch upon the plasticity of other non-β pancreatic cells and their cooperation with β cells to maintain homeostasis.

Insulin's Function in Health and Disease

Insulin is a polypeptide hormone that is primarily released by cells in the pancreatic islets of Langerhans. The hormone may work in tandem with glucagon to control blood sugar levels; glucagon has catabolic properties while insulin has anabolic ones. Insulin controls blood glucose levels and causes the liver, muscles, and adipose tissue to store glucose, which causes total weight gain. Insulin plays a crucial role in the initiation and development of many chronic diseases because it modulates a variety of physiological processes. Other techniques are based on the exogenous infusion of glucose or insulin, or both, either under steady-state (the insulin suppression test) or under dynamic conditions (the insulin tolerance test, intravenous glucose-tolerance test with minimal model analysis, and constant infusion of glucose with model analysis). Homeostatic model assessment uses fasting plasma glucose and insulin concentrations to derive indices of insulin sensitivity and secretion from a mathematical model.

Pancreatic Antioxidative Defense and Heat Shock Proteins Prevent Islet of Langerhans Cell Death After Chronic Oral Exposure to Cadmium LOAEL Dose.

Cadmium, a hazardous environmental contaminant, is associated with metabolic disease development. The dose with the lowest observable adverse effect level (LOAEL) has not been studied, focusing on its effect on the pancreas. We aimed to evaluate the pancreatic redox balance and heat shock protein (HSP) expression in islets of Langerhans of male Wistar rats chronically exposed to Cd LOAEL doses, linked to their survival. Male Wistar rats were separated into control and cadmium groups (drinking water with 32.5 ppm CdCl2). At 2, 3, and 4 months, glucose, insulin, and cadmium were measured in serum; cadmium and insulin were quantified in isolated islets of Langerhans; and redox balance was analyzed in the pancreas. Immunoreactivity analysis of p-HSF1, HSP70, HSP90, caspase 3 and 9, and cell survival was performed. The results showed that cadmium exposure causes a serum increase and accumulation of the metal in the pancreas and islets of Langerhans, hyperglycemia, and hyperinsulinemia, associated with high insulin production. Cd-exposed groups presented high levels of reactive oxygen species and lipid peroxidation. An augment in MT and GSH concentrations with the increased enzymatic activity of the glutathione system, catalase, and superoxide dismutase maintained a favorable redox environment. Additionally, islets of Langerhans showed a high immunoreactivity of HSPs and minimal immunoreactivity to caspase associated with a high survival rate of Langerhans islet cells. In conclusion, antioxidative and HSP pancreatic defense avoids cell death associated with Cd accumulation in chronic conditions; however, this could provoke oversynthesis and insulin release, which is a sign of insulin resistance.

The potential antioxidant effect of N-acetylcysteine on X-ray ionizing radiation-induced pancreas islet cell toxicity

PurposePrevious research has highlighted the impact of X-ray irradiation-induced organ damage, on cancer patients after radiation therapy. The ionizing radiation-induced oxidative stress causes injury to the pancreatic islet cells of Langerhans. We used histopathological, immunohistochemical, and biochemical analyses to examine α- and β-cells in the islets of Langerhans in rats undergoing whole-body x-ray ionizing radiation, a group of which was treated with NAC. Material and methodsTwenty-four male rats were randomly divided into 3 groups, one control, and two experimental groups. Group I (Control) was administered only saline solution (0.09% NaCl) by oral gavage for 7 days. Group II (IR) was administrated whole body single dose 6 Gray ionizing radiation (IR) and saline solution (0.09% NaCl) by oral gavage for 7 days. Group III (IR + NAC) was administered 300 mg/kg NAC (N-acetylcysteine) by oral gavage for 7 days, 5 days before, and 2 days after 6 Gray IR application. ResultsIn the X-ray irradiation group, we observed diffuse necrotic endocrine cells in the islets of Langerhans. In addition, we found that Caspase-3, malondialdehyde (MDA) levels increased, and insulin, glucagon, and glutathione (GSH) levels decreased in the IR group compared to the control group. In contrast, we observed a decrease in Caspase-3, and MDA levels in necrotic endocrine cells, and an increase in insulin, glucagon, and GSH levels in the IR + NAC group compared to the IR group. ConclusionThis study provides evidence for the beneficial effects of N-acetyl cysteine on islets of Langerhans cells with X-ray ionizing-radiation-induced damage in a rat model.

Emerging Anti-Diabetic Drugs for Beta-Cell Protection in Type 1 Diabetes.

Type 1 diabetes (T1D) is a chronic autoimmune disorder that damages beta cells in the pancreatic islets of Langerhans and results in hyperglycemia due to the loss of insulin. Exogenous insulin therapy can save lives but does not halt disease progression. Thus, an effective therapy may require beta-cell restoration and suppression of the autoimmune response. However, currently, there are no treatment options available that can halt T1D. Within the National Clinical Trial (NCT) database, a vast majority of over 3000 trials to treat T1D are devoted to insulin therapy. This review focuses on non-insulin pharmacological therapies. Many investigational new drugs fall under the category of immunomodulators, such as the recently FDA-approved CD-3 monoclonal antibody teplizumab. Four intriguing candidate drugs fall outside the category of immunomodulators, which are the focus of this review. Specifically, we discuss several non-immunomodulators that may have more direct action on beta cells, such as verapamil (a voltage-dependent calcium channel blocker), gamma aminobutyric acid (GABA, a major neurotransmitter with effects on beta cells), tauroursodeoxycholic acid (TUDCA, an endoplasmic reticulum chaperone), and volagidemab (a glucagon receptor antagonist). These emerging anti-diabetic drugs are expected to provide promising results in both beta-cell restoration and in suppressing cytokine-derived inflammation.

Peroxisomes during postnatal development of mouse endocrine and exocrine pancreas display cell-type- and stage-specific protein composition

Peroxisomal dysfunction unhinges cellular metabolism by causing the accumulation of toxic metabolic intermediates (e.g. reactive oxygen species, very -chain fatty acids, phytanic acid or eicosanoids) and the depletion of important lipid products (e.g. plasmalogens, polyunsaturated fatty acids), leading to various proinflammatory and devastating pathophysiological conditions like metabolic syndrome and age-related diseases including diabetes. Because the peroxisomal antioxidative marker enzyme catalase is low abundant in Langerhans islet cells, peroxisomes were considered scarcely present in the endocrine pancreas. Recently, studies demonstrated that the peroxisomal metabolism is relevant for pancreatic cell functionality. During the postnatal period, significant changes occur in the cell structure and the metabolism to trigger the final maturation of the pancreas, including cell proliferation, regulation of energy metabolism, and activation of signalling pathways. Our aim in this study was to (i) morphometrically analyse the density of peroxisomes in mouse endocrine versus exocrine pancreas and (ii) investigate how the distribution and the abundance of peroxisomal proteins involved in biogenesis, antioxidative defence and fatty acid metabolism change during pancreatic maturation in the postnatal period. Our results prove that endocrine and exocrine pancreatic cells contain high amounts of peroxisomes with heterogeneous protein content indicating that distinct endocrine and exocrine cell types require a specific set of peroxisomal proteins depending on their individual physiological functions. We further show that significant postnatal changes occur in the peroxisomal compartment of different pancreatic cells that are most probably relevant for the metabolic maturation and differentiation of the pancreas during the development from birth to adulthood.

The role of the adipose tissue-derived mesenchymal stem cells enriched with melatonin in pancreatic cellular regeneration.

Adipose tissue-derived mesenchymal stem cells (AD-MSCs) were proved to differentiate into insulin-producing cells (IPCs), but the amount of insulin secreted was relatively low compared to the insulin secreted by mature pancreatic islets. Enrichment of MSCs culture with melatonin (MT) was found to promote cartilage matrix synthesis, osteogenic and neuronal differentiation. Therefore, the present study was conducted to evaluate the potential role of MT pre-treated AD-MSCs in enhancing the treatment and regeneration of the islet cells of Langerhans in rats with diabetes induced by streptozotocin (STZ). Forty adult male Sprague Dawley albino rats were divided equally into groups; group I (control group), group II (STZ group), group III (STZ + AD-MSCs) and group IV (STZ+MT pre-treated AD-MSCs). Biochemical studies were implemented including measurements of the body weight, fasting blood glucose and serum insulin levels, Interleukin 17 (IL-17) and IL-10. Samples of the pancreas were taken and prepared for light, fluorescent microscopic examination, proliferating cell nuclear antigen and caspase-3 immunohistochemical studies and histomorphometric analysis. The present study confirmed the regenerative and therapeutic effects of AD-MSCs on the pancreatic cells. Concomitant supply of MT to the culture of AD-MSCs, in group IV, was shown to retain the normal architecture of the islet cells of Langerhans. They appeared well-defined and lightly stained, surrounded by classical pancreatic acini and contained a large number of islet cells with vesicular nuclei and prominent nucleoli. Improvement of all the biochemical parameters, in the same group, was demonstrated by increased body weight and serum insulin levels with a decrease in the fasting blood glucose levels. Significant decrease in the pro-inflammatory cytokine; IL-17 and increase in the anti-inflammatory cytokine; IL-10, compared to the STZ group, were also discovered. Significant increase in the proliferating cell nuclear antigen proliferation index, decrease in caspase-3 and increase in PKH26 labelled MSCs area per cent was recorded in the group of AD-MSCs enriched with MT compared to the group of AD-MSCs without MT. The present study confirmed the potential therapeutic and protective role of MT pre-treated AD-MSCs against the STZ-induced pancreatic islet cells damage. Further studies are recommended to investigate the efficacy of MT and AD-MSCs over longer experimental durations.

Correction to: The effects of β-escin on inflammation, oxidative stress and Langerhans islet cells in high-fat diet and streptozotocin injection induced experimental type-2 diabetes model

Correction to: The effects of β-escin on inflammation, oxidative stress and Langerhans islet cells in high-fat diet and streptozotocin injection induced experimental type-2 diabetes model

The effects of β-escin on inflammation, oxidative stress and Langerhans islet cells in high-fat diet and streptozotocin injection induced experimental type-2 diabetes model

The effects of β-escin on inflammation, oxidative stress and Langerhans islet cells in high-fat diet and streptozotocin injection induced experimental type-2 diabetes model

Bio-engineering of 3-D cell sheets for diabetic rats: Interaction between mesenchymal stem cells and beta cells in functional islet regeneration system

Type 1 diabetes is an autoimmune disease that emerges with the destruction of beta cells of pancreatic Langerhans islets. Three different therapeutical approaches have been developed so far; pancreas transplantation, islet transplantation, and cell-based therapies. Bioengineering cell sheets for tissue generating is one of the latest approaches that have been used to construct cell-sheets instead of single cells so that it mimics the in vivo environments more. In this study, extra-hepatic functional islet tissue was constructed by transferring the 3-D beta cells and GFP labelled MSCs MSC sheets to the subcutaneous site of rats with STZ-induced diabetes. rBM-MSCs and beta cells were cultured on the 6-well PIPAAm culture dishes. Obtained rBM-MSCs as two-cell sheets and beta cells cultured in droplets with matrigel has transplanted into the dorsal subcutaneous area of diabetic rats. Fasting blood glucose levels and body weights were evaluated for 30 days after transplantation. Immunocytochemistry analysis for the anti-apoptotic, anti-inflammatory, and angiogenetic effects of MSCs on the 30th day of subcutaneous cell transplantation. All recipient rats transplanted with beta-cells with MSCs returned toward normoglycemia by day 5 and remained at this level for 30 days. Immunocytochemical analyses supported that the MSCs and beta cells preserved their viability and function. MSCs secrete cytokines and growth factors TGF-β and IL-6; MSCs of the important features of the anti-apoptotic and anti-inflammatory properties, thanks to apoptosis of beta cells preserve graft explained by inhibition. In transplantation of MSCs induced angiogenesis and neovascularization, PECAM-1 and GFP positive simultaneously determining endothelial cells was observed indicating. Subcutaneous 3D beta-cell transplantation would be possible with the MSC-sheets as a feeder layer of beta cells. The beta-cell line is glucose-sensitive and has a high insulin release potential, and can be used as an alternative to islets in in vivo transplant studies.

Primary understanding of type 1 diabetes as an autoimmune disease

Type 1 diabetes (T1D) is classified as an autoimmune disease affecting a wide range of people worldwide. Beta cells in the pancreatic islets of Langerhans in the pancreases are responsible for insulin productions, which help in the exchange of blood glucose into energy. These cells were destroyed by developing particular immune mechanisms. Some newly diagnosed patients with T1D have insignificant scientific understanding of their immune system condition. Importantly, scholars found a direct relationship between hypoglycemic and innate immune response. Therefore, this review was intended to elaborate a simple scientific explanation for T1D, including T1D etiology and pathogenesis, initiation of immune response against β-cell, and immunological impact of the best therapy, in addition to the newest understanding of the cell types and immune mechanisms involved in T1D. This review included articles published from 1997 to 2022 extracted from PubMed, Medline, and Google Scholar databases.

Refractory postoperative Staphylococcus hominis bacteremia in a patient with an ACTH-producing pancreatic neuroendocrine neoplasm: a case report

BackgroundStaphylococcus hominis (S. hominis) is an opportunistic pathogen that is often highly resistant to antibiotics and is difficult to treat. In patients diagnosed with an adrenocorticotropic hormone (ACTH)-producing tumor that compromises the immune system due to hypercortisolemia, cancer treatment and infection control should be considered simultaneously. This report presents a case of refractory postoperative S. hominis bacteremia requiring the prolonged administration of several antibiotics in a patient with an ACTH-producing pancreatic neuroendocrine neoplasm (pNEN).Case presentationA 35-year-old man visited a neighboring hospital for a thorough examination after experiencing weight gain and lower limb weakness for several months. Enhanced computed tomography revealed a pancreatic tail tumor and bilateral adrenal enlargement. Elevated plasma ACTH and serum cortisol were noted. Biopsy under endoscopic ultrasonography revealed the tumor as an ACTH-producing pNEN. The patient was transferred to our hospital for further treatment. Pneumocystis pneumonia was noted and treated with sulfamethoxazole and adjunctive glucocorticoids. Hypercortisolism was controlled with metyrapone and trilostane. Somatostatin receptor scintigraphy and ethoxybenzyl magnetic resonance imaging detected other lesions in the pancreatic head. A total pancreatectomy was performed given that the lesions were found in both the pancreatic head and tail. Plasma ACTH and serum cortisol levels decreased immediately after the resection. Pathological examination revealed that the pancreatic tail tumor was NEN G2 and T3N1aM0 Stage IIB and the pancreatic head lesions were SSTR-positive hyperplasia of the islet of Langerhans cells. On postoperative day 11, catheter-associated bacteremia occurred. Initially, meropenem hydrate and vancomycin hydrochloride were administered empirically. S. hominis was identified and appeared sensitive to these antibiotics according to susceptibility testing. However, S. hominis was repeatedly positive in blood cultures for more than one month, despite treatment with several antibiotics. Eventually, with the combined use of three antibiotics (meropenem hydrate, vancomycin hydrochloride, and clindamycin phosphate) for more than 3 weeks, the S. hominis-associated bacteremia improved. He was discharged 79 days after surgery.ConclusionsOur patient with an ACTH-producing pNEN was immunocompromised and needed meticulous attention for infectious complications even after successful tumor removal. Specifically, S. hominis bacteremia in such patients demands intensive treatments, such as with combinational antibiotics.

Expression and Functional Role of Olfactory, Taste, and Phototransduction Signal Proteins in β Cells in Islets of Langerhans

Expression and Functional Role of Olfactory, Taste, and Phototransduction Signal Proteins in β Cells in Islets of Langerhans

Dividing Cells in Islets of Langerhans Can produce Glucagon

Dividing Cells in Islets of Langerhans Can produce Glucagon

Adding GABA to Insulin leads to new era in Type 1 Diabetes Management

Introduction: Diabetes mellitus is not just a disease, it dramatically affects people's lives, both physically and psychologically. It is like a permanent guest, never leaving its owner. It is promising to know that, it was detected that GABA can stimulate and multiply beta cells in islets of langerhans through activation of PI3K/Akt pathway and can also convert alpha cells to beta cells with long term use. Materials and Methods: 100 patients of type 1 diabetes followed in a private clinic for 1 year. They is on multiple insulin injections in the form of lantus and actrapid. Results: The results show a statistically significant difference in hba1c in patients before and after 6 months of treatment with GABA. Conclusion: GABA is considered as the best choice for adding to insulin for patients with type 1 diabetes decreasing insulin dose, decreasing incidence of diabetes complications.

Antioxidative, Antidiabetic, and Hypolipidemic Properties of Probiotic-Enriched Fermented Camel Milk Combined with Salvia officinalis Leaves Hydroalcoholic Extract in Streptozotocin-Induced Diabetes in Rats.

Antioxidative, antidiabetic, and hypolipidemic properties of probiotic-enriched fermented camel milk (FCM) combined with Salvia officinalis L. leaves hydroalcoholic extract (SOHE) in streptozotocin-induced diabetes in rats were investigated. Phytochemicals analysis and antioxidant capacity indicated that S. officinalis contained high phenolics with super antioxidant activity. Subsequently, HPLC analysis demonstrated 13 phenolic acids and 14 flavonoids in considerable amounts with ferulic acid and resveratrol as predominant, respectively. The antidiabetic and hypolipidemic properties of FCM and SOHE were examined in a designed animal model consisting of seven treated groups for four weeks. There was a negative group (G1); the positive group (G2) received a single dose (50 mg kg−1) of streptozotocin (STZ) by intraperitoneal injection (i.p.); in G3, diabetic rats (DRs) orally received 5 mL FCM kg−1 daily; in G4, DRs orally received 50 mg GAE SOHE kg−1 daily; in G5, DRs orally received 5 mL FCM contains 25 mg GAE SOHE kg−1 daily; in G6, DRs orally received 5 mL FCM contains 50 mg GAE SOHE kg−1 daily; in G7, DRs orally received 50 mg metformin kg−1 daily. Combining FCM with SOHE at 25 or 50 mg kg−1 exhibited a synergistic effect in significantly lowering random blood glucose (RBG), fasting blood glucose (FBG), and improved weight gain recovery %. The hypolipidemic effect of FCM + 50 mg GAE SOHE kg−1 was significantly higher than using FCM or SOHE individually, and attenuation in triglycerides (TG), total cholesterol (CHO), and high- and low-density lipoproteins (HDL and LDL), and very-low-density lipoproteins (VLDL) was remarked. Combining FCM with SOHE at 25 or 50 mg kg−1 ameliorated liver and kidney functions better than individual uses of FCM, SOHE, or metformin. Interestingly, FCM with 50 mg SOHE kg−1 presented significant improvement in the activity of antioxidant enzymes, reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), and a substantial reduction in malonaldehyde (MDA) levels with 53.75%, 89.93%, 63.06%, and 58.69% when compared to the STZ group (G2), respectively. Histopathologically, administrating FCM + 25, 50 mg SOHE kg−1 or 50 mg kg−1 metformin showed a normal histological structure of both islets of Langerhans cells and acini. In conclusion, combining FCM with SOHE presented synergistic and therapeutical efficacy. It could be beneficial and profitable for controlling diabetes mellitus complications and protecting against oxidative stress.

Experimental model of unpredictable maternal stress and diabetes risk of offspring: An immunohistochemical study

The effect of stress on the occurrence of diabetes mellitus (DM) is commonly reported in recent studies. Maternal stress may have a negative effect on the later life of offspring. However, most studies only investigated long-term intrauterine stress on behavioral, emotional, psychological, and immunological disorders of offspring. The relationship between maternal stress and DM occurrence in the later life period of offspring is not known. This rat model study aimed to evaluate the susceptibility of offspring to DM after exposure to intrauterine stress. The purpose of this study is to examine serum glucose levels of mothers and offspring exposed to maternal stress and to evaluate pancreatic tissues pathologically and immunohistochemically. Twelve, Wistar Albino female rats were equally divided into two groups: controls and maternal stress groups. Normal routine conditions were applied to the control group without any stress. The pregnant rats in the maternal stress group were exposed to chronic unpredictable stressors throughout the 21-day gestation. One female and one male offspring and mothers from each term delivery were randomly selected and euthanatized at the 35th day. During the necropsy, blood and pancreatic tissue samples were collected from both mothers and pups. High serum glucose levels from mothers and offspring in the maternal stress group and the control group were compared. Additionally, histopathological examinations assessed the increased cell degeneration in mother rats and offspring. Immunohistochemical examinations revealed decreased insulin, amylin, and insulin receptor expressions and slightly increased glucagon expression in Langerhans islet cells in the maternal stress group. These results indicated that maternal stress may be a predisposing factor for DM in both mothers and offspring in their later life periods.

Physically interacting beta-delta pairs in the regenerating pancreas revealed by single-cell sequencing

ObjectivesUntil recently, communication between neighboring cells in islets of Langerhans was overlooked by genomic technologies, which require rigorous tissue dissociation into single cells. MethodsWe utilize sorting of physically interacting cells (PICs) with single-cell RNA-sequencing to systematically map cellular interactions in the endocrine pancreas after pancreatectomy. ResultsThe pancreas cellular landscape features pancreatectomy associated heterogeneity of beta-cells, including an interaction-specific program between paired beta and delta-cells. ConclusionsOur analysis suggests that the particular cluster of beta-cells that pairs with delta-cells benefits from stress protection, implying that the interaction between beta- and delta-cells might safeguard against pancreatectomy associated challenges. The work encourages testing the potential relevance of physically-interacting beta-delta-cells also in diabetes mellitus.

Covid-19 Induced Diabetes: Disclosing Truth behind the Potential Attention Seeker

<p style="text-align: justify;">Severe Acute Respiratory Syndrome Corona Virus-2 (SARS-CoV-2), the zoonotic virus answerable for the current global health crisis is ringing its dangerous bells on its post disease status. COVID-19 is causing multiple organ damage probably with its entry site. Insulin-Dependent Diabetes (IDDM) also known as Type I Diabetes is a multifactorial disease that typically occurs as a result of the interaction of genetic, environmental and immunologic factors. The mechanisms behind the development of Diabetes and associated consequences are complicated. The morphological mass of Insulin producing &beta;-cells in the pancreatic islets of Langerhans and the functional status determine plasma Insulin levels. Insufficient Insulin levels may develop as a result of a lack of &beta;-cell function resulting in hyperglycemia and Diabetes. <em>Angiotensin-Converting Enzyme 2</em> (ACE2) receptor, the binding agent which allows Corona virus to enter and migrate to various organs such as lungs, heart, liver, pancreas, and kidneys is assumed to be responsible for this damage. The over expression of ACE2 receptor on pancreatic endocrine cells paves a way for extensive damage to Islets of Langerhans causing Insulin resistance and deficiency. Another common assumption among the researchers and health care professionals are the dreadful relationship shared by viruses and Diabetes which can exacerbate or provoke autoimmunity leading to &beta;-cell auto-oxidation. The metabolic complications like Diabetic Ketoacidosis (DKA) and Hyper osmolar hyperglycemia are predominantly seen in various regions of the world in people with Pre-Diabetes and non-diabetics. However, this review explored the probable truth behind COVID-19 induced new-onset Diabetes mellitus and its complications. <strong>Key words:</strong> COVID -19, Type-1 Diabetes, ACE2 receptor, Diabetic, Ketoacidosis.