Implications Of Diabetes Mellitus Research Articles

Recurrence risk analysis for stage II and III colorectal cancer, and the implications of diabetes mellitus as a risk factor for the recurrence of stage III colorectal cancer.

The present study investigated the risk factors for recurrence in patients with stage II-III colorectal cancer (CRC) who underwent colorectal surgery. Data from 232 patients with stage II and III CRC who underwent primary tumor resection were retrospectively analyzed. Univariate and multivariate analyses were performed to determine the risk factors for recurrence. The overall recurrence rate was 21.6% (n=50/232). Univariate Cox regression analysis identified diabetes mellitus (DM) (P=0.032) as a risk factor for recurrence. In addition, multivariate Cox regression analysis showed that DM was an independent risk factor for recurrence-free survival (RFS) (hazard ratio 2.40, P=0.016). The RFS curve obtained using the Kaplan-Meier method indicated that in patients with stage III colon cancer, the non-DM group demonstrated a significantly longer RFS than the DM group (P=0.012). In conclusion, the present study demonstrated that DM may be an independent risk factor for recurrence in patients undergoing curative resection for stage III CRC. Consequently, better postoperative therapy and careful monitoring might be required, especially in patients with stage III CRC and preoperative DM.

A Network Pharmacology-based Approach to Explore Potential Targets and Mechanism of Berberis aristata Focusing on its Implications for Diabetes Mellitus

Berberis aristata, a revered medicinal shrub in traditional systems like Ayurveda, holds promise in managing diabetes mellitus, a burgeoning global health concern. Through a comprehensive analysis of its bioactive compounds and their interactions with potential targets, this study elucidates the molecular mechanisms underlying its anti-diabetic effects. Screening through databases yielded 17 bioactive compounds, including rutin, quercetin, and berberine. Protein-protein interaction analysis identified 44 potential targets, with 36 genes overlapping with disease-related genes, indicating pivotal pathways in diabetes mellitus treatment. Further, pathway analysis highlighted G-protein coupled receptor signaling, calcium signaling, and neurotransmitter receptor activity as significant, with adjusted p-values. Network analysis revealed key hub genes like DRD1 and MMP2, emphasizing their central role in Berberis aristata’s therapeutic action. The findings underscore Berberis aristata’s potential as a source of novel anti-diabetic agents and offer groundwork for potential research in this field.

A Bidirectional Immunological Relationship between Diabetes Mellitus and Tuberculosis: A Narrative Review

Tuberculosis (TB) is one of the most common contagious diseases worldwide. Over the past few decades, researchers have made significant efforts to prevent TB. Recent predictions indicate that the prevalence of Diabetes Mellitus (DM) will reach 552 million by 2023 due to ongoing epidemiological changes in several countries across the globe. India is expected to have 62-80 million people with diabetes by 2030, making it the "Diabetes Capital" of the world. Present review discusses the urgent need to understand the mechanisms and implications of DM on the immune systems of TB patients. The correlation between TB and DM has been shown to be bidirectional. Numerous studies have revealed a higher prevalence of diabetes in TB patients, as their immune systems are compromised. TB patients with DM experience progressive deficits in both innate and adaptive immune cell activity, reducing their ability to suppress Mycobacterium tuberculosis (M. tuberculosis) and increasing their risk of developing TB. Increased inflammation and elevated levels of inflammatory cytokines in circulation are characteristics of TB with DM co-morbidity, which indicate the active involvement of the angiogenesis-inflammation nexus. Therefore, to alleviate the burden of both disorders, it would be beneficial to make informed therapy choices by gaining a better understanding of TB immunology in the context of DM.

Normal-weight central obesity: implications for diabetes mellitus.

Current guidelines for obesity prevention and control focus on body mass index (BMI) and rarely address central obesity. Few studies have been conducted on the association between normal-weight central obesity and the risk of diabetes mellitus (DM). 26,825 participants from the National Health and Nutrition Examination Survey (NHANES) were included in our study. A weighted multivariate logistic regression model was used to analyze the relationship between different obesity patterns and the risk of DM. Our results suggest that normal-weight central obesity is associated with an increased risk of DM (OR: 2.37, 95% CI: 1.75-3.23) compared with normal-weight participants without central obesity. When stratified by sex, men with normal-weight central obesity, obesity and central obesity were found to have a similar risk of DM (OR: 3.83, 95% CI: 2.10-5.97; OR: 4.20, 95% CI: 3.48-5.08, respectively) and a higher risk than all other types of obesity, including men who were overweight with no central obesity (OR: 1.21, 95% CI: 0.96-1.51) and obese with no central obesity (OR: 0.53, 95% CI: 0.30-0.91). Our results highlight the need for more attention in people with central obesity, even if they have a normal BMI.

Arginase: Biological and Therapeutic Implications in Diabetes Mellitus and Its Complications.

Arginase is a ubiquitous enzyme in the urea cycle (UC) that hydrolyzes L-arginine to urea and L-ornithine. Two mammalian arginase isoforms, arginase1 (ARG1) and arginase2 (ARG2), play a vital role in the regulation of β-cell functions, insulin resistance (IR), and vascular complications via modulating L-arginine metabolism, nitric oxide (NO) production, and inflammatory responses as well as oxidative stress. Basic and clinical studies reveal that abnormal alterations of arginase expression and activity are strongly associated with the onset and development of diabetes mellitus (DM) and its complications. As a result, targeting arginase may be a novel and promising approach for DM treatment. An increasing number of arginase inhibitors, including chemical and natural inhibitors, have been developed and shown to protect against the development of DM and its complications. In this review, we discuss the fundamental features of arginase. Next, the regulatory roles and underlying mechanisms of arginase in the pathogenesis and progression of DM and its complications are explored. Furthermore, we review the development and discuss the challenges of arginase inhibitors in treating DM and its related pathologies.

Self-reported memory problems in adult-onset cancer survivors in the United States with or without: Type 2 diabetes mellitus, hypertension and hyperlipidemia.

e24062 Background: Cancer and chronic diseases (CD) are independent predictors of cognitive dysfunction, especially memory problems that can impact patients’ psychosocial functioning and quality of life. We examined the prevalence of memory problems in cancer patients with or without CD, including Type 2 Diabetes mellitus (DM), hypertension (HTN) and hyperlipidemia (HLD). Methods: We examined data from people who completed the US National Health and Nutrition Examination Survey from 2009 to 2016 to determine the prevalence of memory problems in cancer survivors vs. non-cancer survivors with and without a history of CD. Participants answered the ‘yes’ or ‘no’ question: “Are you limited in any way because of difficulty remembering or because you experience periods of confusion?” History of Cancer, DM, HTN and HLD were self-reported. We used Rao-Scott Modified Chi-Square Test (X2test) for cross-classified categorical data from complex sample survey. Age, sex, race-ethnicity, education, poverty, and general health were controlled using logistic regression. Results: The sample included 21813 adults, ³ 20 years old, and ≈52% female. There were 40% Whites, 22% Blacks, 25% Mexican American/Other Hispanics, and 13% other race/multi-racial. About 46% graduated high School/had a GED (21.2%) or completed less than high school (24.4%). Of those with cancer ( N= 2025), memory problems were associated with DM (17.72%; X2test, p= 0.003) and (HTN, 13.42%; X2test, p= 0.007), but not HLD (11.66%; X2test, p= 0.786). Of those without cancer, memory problems were associated with DM, HTN and HLD (all p< 0.0001). Prevalence of CD was much greater in cancer survivors with memory problems ( p< .05). Conclusions: Strategies to mitigate memory problems in cancer survivors should consider the implications of DM, HTN and HLD, particularly given the prevalence of these chronic morbidities in cancer populations.

Implications of Diabetes Mellitus in Patients with Acute Coronary Syndromes - Poorer Outcomes Among Diabetics

Abstract Cardiovascular disease is the leading cause of death in the world, causing over 17 million deaths annually, of which 7.2 million by coronary heart disease. They are a major public health problem worldwide, of which acute coronary syndromes show special attention due to increased prevalence and incidence and poor prognosis. Although advanced therapies can improve the morbidity and mortality associated with acute coronary syndromes in well-developed countries, developing countries remain exposed to the ravages of these diseases. Of the patients admitted for acute coronary syndrome, about 30% suffer from diabetes mellitus, considered a major risk factor and a predictor for unfavorable evolution regardless of the type of acute coronary syndrome.

Vanadium in Biological Action: Chemical, Pharmacological Aspects, and Metabolic Implications in Diabetes Mellitus

Vanadium compounds have been primarily investigated as potential therapeutic agents for the treatment of various major health issues, including cancer, atherosclerosis, and diabetes. The translation of vanadium-based compounds into clinical trials and ultimately into disease treatments remains hampered by the absence of a basic pharmacological and metabolic comprehension of such compounds. In this review, we examine the development of vanadium-containing compounds in biological systems regarding the role of the physiological environment, dosage, intracellular interactions, metabolic transformations, modulation of signaling pathways, toxicology, and transport and tissue distribution as well as therapeutic implications. From our point of view, the toxicological and pharmacological aspects in animal models and humans are not understood completely, and thus, we introduced them in a physiological environment and dosage context. Different transport proteins in blood plasma and mechanistic transport determinants are discussed. Furthermore, an overview of different vanadium species and the role of physiological factors (i.e., pH, redox conditions, concentration, and so on) are considered. Mechanistic specifications about different signaling pathways are discussed, particularly the phosphatases and kinases that are modulated dynamically by vanadium compounds because until now, the focus only has been on protein tyrosine phosphatase 1B as a vanadium target. Particular emphasis is laid on the therapeutic ability of vanadium-based compounds and their role for the treatment of diabetes mellitus, specifically on that of vanadate- and polioxovanadate-containing compounds. We aim at shedding light on the prevailing gaps between primary scientific data and information from animal models and human studies.

Netrin as a Novel Biomarker and Its Therapeutic Implications in Diabetes Mellitus and Diabetes-Associated Complications.

Diabetes is a multifactorial metabolic syndrome and is one of the shared long-lasting illnesses globally. It is linked to long-term microvascular and macrovascular complications that contribute to disability, compromised quality of life, and reduction in lifespan, which eventually leads to death. This disease is not only incurring significant economic burden but also adversely affects the patients, caregivers, communities, and the society at large. The interruption of diabetes progress and its complications is a primary focus of scientific communities. In spite of various diagnostic modalities for diabetes, there is a limited marker to investigate the risk and progress of its complications. Netrin has recently received more attention as a biomarker of diabetes and a broader range of long-term complication. Therefore, the impetus of this review is to exhaustively discuss the role of Netrin as a potential biomarker and its therapeutic implication in diabetes and diverse sets of microvascular and macrovascular complications of diabetes. It also discourses the possible mechanisms of Netrin for the said pharmacological effect for a better understanding of the development and progression of diabetes and its complications in relation to this protein. It enables protective measures to be applied at the subclinical stage and the responses to preventive or therapeutic measures to be scrutinized. Besides, it might also facilitate the appraisal of novel therapeutic options for diabetes and various complications through modifying the endogenous Netrin and provide surrogate endpoints for intervention.

The Implications of Diabetes Mellitus on the Pattern of Risk factors Profile and treatment strategies in Patients with Acute Coronary Syndrome

The Implications of Diabetes Mellitus on the Pattern of Risk factors Profile and treatment strategies in Patients with Acute Coronary Syndrome

Biophysical and immunological characterization of 2-dRib modified HSA and its implications in diabetes mellitus

Glycoxidation of protein may lead to develop diabetes. In the present study, different concentrations of 2-deoxy d-ribose (2-dRib) were used to modify human serum albumin (HSA). Nitro Blue Tetrazolium (NBT) assay results showed that yield of the fructosamine content was directly proportional to the concentration of 2-dRib. UV and fluorescence spectroscopy results showed an increment in hyperchromicity and decrease in fluorescence intensity of 2-dRib modified HSA as compared to native HSA. Further secondary structural changes were confirmed by UV-circular dichroism (UV-CD) and Fourier transform infrared spectroscopy (FT-IR). To evaluate the immunogenicity of 2-dRib modified HSA, rabbits were immunized with native and 2-dRib modified HSA. Modified HSA sera showed high antibodies titre as compared to native HSA. Moreover, the binding affinity of native and modified HSA with diabetic patient's sera has been evaluated by direct binding ELISA. It was found that diabetic patient's sera showed high binding affinity with the modified HSA as compared to native HSA. On the basis of above findings, it can be concluded that 2-dRib is a potential glycating agent that can cause alteration in HSA structure and make HSA more immunogenic that might play a role in onset and progression of diabetes mellitus and its complications.

Unraveling the aggregation propensity of human insulin C-peptide.

Over the last 20 years, proinsulin C-peptide emerged as an important player in various biological events. Much time and effort has been spent in exploring all functional features of C-peptide and recording its implications in Diabetes mellitus. Only a few studies, though, have addressed C-peptide oligomerization and link this procedure with Diabetes. The aim of our work was to examine the aggregation propensity of C-peptide, utilizing Transmission Electron Microscopy, Congo Red staining, ATR-FTIR, and X-ray fiber diffraction at a 10 mgml-1 concentration. Our experimental work clearly shows that C-peptide self-assembles into amyloid-like fibrils and therefore, the aggregation propensity of C-peptide is a characteristic novel feature that should be related to physiological and also pathological conditions. © 2016 Wiley Periodicals, Inc. Biopolymers (Pept Sci) 108: 1-8, 2017.

Metabolic control of the proteotoxic stress response: implications in diabetes mellitus and neurodegenerative disorders.

Proteome homeostasis, or proteostasis, is essential to maintain cellular fitness and its disturbance is associated with a broad range of human health conditions and diseases. Cells are constantly challenged by various extrinsic and intrinsic insults, which perturb cellular proteostasis and provoke proteotoxic stress. To counter proteomic perturbations and preserve proteostasis, cells mobilize the proteotoxic stress response (PSR), an evolutionarily conserved transcriptional program mediated by heat shock factor 1 (HSF1). The HSF1-mediated PSR guards the proteome against misfolding and aggregation. In addition to proteotoxic stress, emerging studies reveal that this proteostatic mechanism also responds to cellular energy state. This regulation is mediated bythe key cellular metabolic sensor AMP-activated protein kinase (AMPK). In this review, we present an overview of the maintenance of proteostasis by HSF1, the metabolic regulation of the PSR, particularly focusing on AMPK, and their implications in the two major age-related diseases-diabetes mellitus and neurodegenerative disorders.

Microcystin-LR induces dysfunction of insulin secretion in rat insulinoma (INS-1) cells: Implications for diabetes mellitus

Microcystins (MCs) are the most frequent cyanobacterial toxins observed in freshwater systems. Accumulating evidence suggests that MCs pose a serious threat to public health. However, the contributions of the exposure of MCs to the occurrence of human diseases remain largely unknown. This study provides the evidence of the effects of MC-LR on pancreatic β-cell function through the exposure of rat insulinoma (INS-1) cells to 0, 10, 20, or 40μM MC-LR for 72h and explores the underlying molecular mechanisms. Our results demonstrate that exposure to MC-LR for 72h suppresses cell viability, disturbs glucose-stimulated insulin secretion (GSIS), and decreases the expression of insulin protein. Moreover, MC-LR disrupts the cell cycle distribution and increases cell apoptosis at 20 or 40μM for 72h, respectively, indicating that the β-cell mass would be decreased by MC-LR exposure. A transcriptomic analysis revealed several key genes (e.g., Pdx-1, Neurod1, and Abcc8) involved in insulin secretion are significantly differentially expressed in INS-1 cells in response to MC-LR exposure. In addition, several signal transduction pathways associated with diabetes (e.g., type 1 and 2 diabetes) were also identified compared with the control cells. We recommend that MC be considered as a new environmental factor that promotes diabetes development. The identified key genes or pathways may potentially contribute to the future therapies in the environmental contaminants induced β-cell damage.

Assimilating the impact of diabetes mellitus in children under the perspective of mothers

Aimed at assimilating the impact of diabetes mellitus in children and in the family life under the perspective of the primary caregiver. Descriptive qualitative research conducted with seven mothers in a center of reference in Crato, CE, Brazil in the months of June and July, 2011. With these major thematic categories: characterization of family caregivers; implications of diabetes mellitus in the child's life under the perspective of the mother; family experience facing diabetes. Behavioral changes in children such as aggressiveness, feelings of denial and fear were assimilated. It was also observed that the care of diabetic children falls back on the mother. Thus, we see the need to implement a multidisciplinary, interdisciplinary and humanized care, aimed at patients with diabetes mellitus and their caregivers, with emphasis on health education.

Novel pathway of iron‑induced blood coagulation: implications for diabetes mellitus and its complications

Fibrinogen (FBG) is a high-molecular-weight protein and precursor to the enzymatically formed fibrin. It has been recently discovered that FBG can be converted into an insoluble, fibrin-like polymer by a nonenzymatic action of hydroxyl radicals (HRs). These free radicals are generated due to the reaction between hydroxyl groups of water and trivalent ferric ions without the participation of any redox agent. The interaction between HRs and FBG occurs in a purified system, as well as in human plasma and in whole blood. Scanning electron microscopy (SEM) of thrombin-induced fibers and those generated with ferric chloride has shown substantial differences in their morphology and susceptibility to enzymatic degradation. Fibrin strands caused by thrombin are thick and easily digested with chymotrypsin. By contrast, the dense matted deposits formed from FBG in the presence of ferric ions are remarkably resistant to proteolytic and chemical degradations due to the presence of intermolecular hydrophobic bonds. Thus, we postulate that this iron-catalyzed reaction represents a novel blood coagulation pathway operating in degenerative diseases. By means of SEM, we showed the presence of dense fibrin-like deposits in the blood of diabetic patients. Therefore, the prothrombotic state and cardiovascular complications observed in diabetes can be explained in terms of the persistent in vivo action of free iron. This phenomenon may explain hemorheologic disturbances in patients with metabolic syndrome and other diseases caused by iron overload. Of note, HRs can be effectively scavenged by phenolic substances; therefore, certain natural polyphenolic substances, which also scavenge HRs, may be considered to have a potential antidiabetic effect. Moreover, natural or synthetic iron-binding substances may also be considered as a new class of antidiabetic drugs.

Restoring Erectile Function by Antioxidant Therapy in Diabetic Rats

Diabetes mediates an increase in reactive oxygen species that can lead to impaired endothelial function, decreased smooth muscle in the diabetic corpus cavernosum and increased apoptosis. We hypothesized that antioxidant therapy may restore erectile function by inhibiting apoptosis in diabetic rat crura. A total of 40 male Sprague-Dawley rats were randomized to 5 groups of 8 each, including healthy controls, rats with diabetes, and rats with diabetes with the antioxidant tempol (4-hydroxytetramethyl-piperidine-1-oxyl) (Sigma-Aldrich), with insulin, and with tempol and insulin. Intracavernous pressure was measured for functional analysis. Smooth muscle and collagen fiber levels in the rat penile corpus cavernosum were assessed by hematoxylin and eosin, and Masson's trichrome staining. Endothelial cells were assessed by CD31 staining. Reactive oxygen species related genes were analyzed by cDNA microarray. We confirmed mRNA and protein expression profiles for these genes in diabetic and treated rats using real-time reverse transcriptase-polymerase chain reaction and immunohistochemistry. TUNEL assay was done to analyze apoptosis status. Intracavernous pressure in diabetic rats was significantly decreased vs controls. After treatment with tempol or insulin alone intracavernous pressure was significantly increased compared to that in untreated diabetic rats. In the diabetic group mean smooth muscle area significantly decreased but was restored after combined tempol and insulin. Endothelial cell area in diabetic rats significantly decreased and was not restored by any treatments. However, apoptosis was restored to normal by combined insulin and tempol. Of 84 reactive oxidative stress and antioxidant genes 32 were identified specific to diabetic rats compared to healthy controls. UCP3 expression was significantly increased in diabetic rats and normal levels were restored by all treatments. To our knowledge this is the first report that tempol and insulin can restore erectile function in diabetic rats by inhibiting apoptosis.

Effects of coronary artery disease and percutaneous intervention on the cardiac metabolism of nonesterified fatty acids and insulin: Implications of diabetes mellitus

Nonesterified fatty acids (NEFA) and insulin have been implicated in the pathogenesis of diabetes mellitus (Type 2 diabetes) and coronary artery disease (CAD). We hypothesized that intracardiac levels of insulin and NEFA within the aortic root, coronary sinus and systemic venous levels would be different in patients with coronary atherosclerosis and/or diabetes. We also studied the metabolic cardiac response following percutaneous coronary intervention (PCI). A total of 67 subjects (42 males; mean age 60 +/- 11 years) were recruited, of which three groups were identified: Group I - those with no CAD or Type 2 diabetes (n = 17); Group II - those with CAD but no Type 2 diabetes (n = 40); and Group III - patients with Type 2 diabetes and CAD (n = 10). Of the whole cohort, 34 patients (51%) proceeded to PCI. NEFA and insulin levels were analysed using enzymatic colorimetric and a monoclonal immuno-autoanalyser techniques, respectively. Subsequently, fractional extraction (FFE) of both variables was calculated. Nonesterified fatty acids and insulin concentrations were lower in the aortic root versus coronary sinus (both P < 0.05). FFE of NEFA was 2x higher in Group I (P < 0.01) with a sevenfold reduction in insulin FFE in Group III. Following PCI, systemic NEFA levels increased significantly (P < 0.05) with no significant change seen within the coronary sinus (P = NS), whilst a reduction in insulin concentrations at all three sites was observed (all P < 0.01). No significant difference in FFE of NEFA was seen after PCI when comparing Groups II and III. There was a drop in insulin extraction in Group II (nondiabetic subjects, from 12% to -4%, P = 0.04), compared with an increase seen in Group III (Type 2 diabetes patients, from -4% to 3%, P = 0.03). There is an intracardiac gradient of NEFA and insulin in Groups I-III. Cardiac NEFA metabolism was higher in those with mild CAD compared with those with obstructive CAD whereas intracardiac insulin extraction was lower in Group III (diabetic) patients. PCI was associated with a systemic rise in NEFA, with a reduction in insulin levels and cardiac utilization, but these effects were blunted in diabetic patients.

Induction of paraoxonase 1 and apolipoprotein A-I gene expression by aspirin

Low-dose aspirin therapy has become a standard in the treatment of cardiovascular diseases. Aspirin has been shown to inhibit atherosclerosis in mouse models. To determine the mechanisms by which aspirin might inhibit atherosclerosis, we incubated HEPG2 cells and rat primary hepatocytes with aspirin or salicylic acid and noted an increase in paraoxonase 1(PON1) activity in the medium, together with an induction of PON1 and apolipoprotein A-I (apoA-I) gene expression. Mice treated with aspirin also showed a 2-fold increase in plasma PON1 activity and a significant induction of both PON1 and apoA-I gene expression in the liver. The induction of the PON1 gene in cell culture was accompanied by an increase in arylhydrocarbon receptor (AhR) gene expression. Accordingly, aspirin treatment of AhR(-/-) animals failed to induce PON1 gene expression. We previously suggested that aspirin might be hydrolyzed by serum PON1, which could account for its short plasma half-life of 10 min. Taken together with the current studies, we suggest that the antiatherosclerotic effects of aspirin might be mediated by its hydrolytic product salicylate and that the induction of PON1 and apoA-I might be important in the cardioprotective effects of aspirin.

Impact of diabetes mellitus on outcomes of superficial femoral artery endoluminal interventions

Although aggressive endoluminal therapy for superficial femoral artery (SFA) occlusive disease is commonplace, the implications of diabetes mellitus (DM) on long-term outcomes in this population are unclear. We examined the consequences of endovascular treatment of the SFA in patients with and without DM. A database of patients undergoing endovascular treatment of the SFA between 1986 and 2005 was maintained. Three groups were defined: nondiabetic patients, those with non-insulin-dependent DM (NIDDM), and those with insulin-dependent DM (IDDM). Intention-to-treat analysis was performed. Results were standardized to TransAtlantic Inter-Society Consensus (TASC) and Society for Vascular Surgery criteria. Time-dependent outcomes were assessed with Kaplan-Meier survival analyses. Factor analyses were performed using a Cox proportional hazard model for time-dependent variables. Data are presented as mean +/- SD where appropriate. Endovascular treatment (ie, balloon angioplasty +/- adjuvant stenting in 38%) was initiated in 525 limbs in 437 patients (68% male; average age, 66 +/- 14 years) for claudication failing conservative therapy or chronic critical limb ischemia (CLI). Of these, 50% were nondiabetic, 26% had NIDDM, and 24% had IDDM. Analyses were separated by those presenting with claudication (61%) and those presenting with CLI (39%). Among patients presenting with claudication, those with IDDM had significantly lower assisted primary patency (P < .01) and a higher incidence of restenosis (P = .04). Patencies at 3 years for nondiabetic, NIDDM, and IDDM were 62%, 72%, and 54% (primary), and 81%, 86%, and 65% (assisted primary), respectively. Patency and restenosis rates were associated with lesion calcification, TASC D lesion categorization, and acute periprocedural occlusion. Among patients presenting with CLI, patency and restenosis rates were equivalent across all groups; however, limb salvage was significantly worse for both groups of diabetic patients compared with nondiabetic (NIDDM, P = .01; IDDM, P = .02). Reduction in limb salvage rates was associated with presence of tissue loss at presentation, end-stage renal disease, and progression of distal disease on follow-up. Endoluminal therapy for SFA occlusive disease yields lower assisted patency rates and higher restenosis rates for those patients presenting with claudication who have more advanced diabetes (ie, IDDM). Among those patients presenting with CLI, particularly those with tissue loss, limb salvage rates are lowered for the diabetic groups (NIDDM and IDDM) despite equivalent patency and restenosis rates.