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Efficacy of a pharmacist-managed diabetes clinic in high-risk diabetes patients, a randomized controlled trial - "Pharm-MD" : Impact of clinical pharmacists in diabetes care.
Halalau, A, Sonmez, M, Uddin, A, Karabon, P, Scherzer, Z, Keeney, S
BMC endocrine disorders. 2022;(1):69
Abstract
BACKGROUND Diabetes mellitus affects 13% of American adults. To address the complex care requirements necessary to avoid diabetes-related morbidity, the American Diabetes Association recommends utilization of multidisciplinary teams. Research shows pharmacists have a positive impact on multiple clinical diabetic outcomes. METHODS Open-label randomized controlled trial with 1:1 assignment that took place in a single institution resident-run outpatient medicine clinic. Patients 18-75 years old with type 2 diabetes mellitus and most recent HbA1c ≥9% were randomized to standard of care (SOC) (continued with routine follow up with their primary provider) or to the SOC + pharmacist-managed diabetes clinic PMDC group (had an additional 6 visits with the pharmacist within 6 months from enrollment). Patients were followed for 12 months after enrollment. Data collected included HbA1c, lipid panel, statin use, blood pressure control, immunization status, and evidence of diabetic complications (retinopathy, nephropathy, neuropathy). Intention-to-treat and per-protocol analysis were performed. RESULTS Forty-four patients were enrolled in the SOC + PMDC group and 42 patients in the SOC group. Average decrease in HbA1c for the intervention compared to the control group at 6 months was - 2.85% vs. -1.32%, (p = 0.0051). Additionally, the odds of achieving a goal HbA1c of ≤8% at 6 months was 3.15 (95% CI = 1.18, 8.42, p = 0.0222) in the intervention versus control group. There was no statistically significant difference in the remaining secondary outcomes measured. CONCLUSIONS Addition of pharmacist managed care for patients with type 2 diabetes mellitus is associated with significant improvements in HbA1c compared with standard of care alone. Missing data during follow up limited the power of secondary outcomes analyses. TRIAL REGISTRATION ClinicalTrials.gov , ID: NCT03377127 ; first posted on 19/12/2017.
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Impact of Sodium-Glucose Co-Transporter 2 Inhibitors on Cardiac Protection.
Wu, VC, Li, YR, Wang, CY
International journal of molecular sciences. 2021;(13)
Abstract
Sodium-glucose co-transporter 2 (SGLT2) inhibitors have been approved as a new class of anti-diabetic drugs for type 2 diabetes mellitus (T2DM). The SGLT2 inhibitors reduce glucose reabsorption through renal systems, thus improving glycemic control in all stages of diabetes mellitus, independent of insulin. This class of drugs has the advantages of no clinically relevant hypoglycemia and working in synergy when combined with currently available anti-diabetic drugs. While improving sugar level control in these patients, SGLT2 inhibitors also have the advantages of blood-pressure improvement and bodyweight reduction, with potential cardiac and renal protection. In randomized control trials for patients with diabetes, SGLT2 inhibitors not only improved cardiovascular and renal outcomes, but also hospitalization for heart failure, with this effect extending to those without diabetes mellitus. Recently, dynamic communication between autophagy and the innate immune system with Beclin 1-TLR9-SIRT3 complexes in response to SGLT2 inhibitors that may serve as a potential treatment strategy for heart failure was discovered. In this review, the background molecular pathways leading to the clinical benefits are examined in this new class of anti-diabetic drugs, the SGLT2 inhibitors.
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Beneficial effects of cinnamon and its extracts in the management of cardiovascular diseases and diabetes.
Shang, C, Lin, H, Fang, X, Wang, Y, Jiang, Z, Qu, Y, Xiang, M, Shen, Z, Xin, L, Lu, Y, et al
Food & function. 2021;(24):12194-12220
Abstract
Cardiovascular diseases (CVDs) and diabetes are the leading causes of death worldwide, which underlines the urgent necessity to develop new pharmacotherapies. Cinnamon has been an eminent component of spice and traditional Chinese medicine for thousands of years. Numerous lines of findings have elucidated that cinnamon has beneficial effects against CVDs in various ways, including endothelium protection, regulation of immune response, lowering blood lipids, antioxidative properties, anti-inflammatory properties, suppression of vascular smooth muscle cell (VSMC) growth and mobilization, repression of platelet activity and thrombosis and inhibition of angiogenesis. Furthermore, emerging evidence has established that cinnamon improves diabetes, a crucial risk factor for CVDs, by enhancing insulin sensitivity and insulin secretion; regulating the enzyme activity involved in glucose; regulating glucose metabolism in the liver, adipose tissue and muscle; ameliorating oxidative stress and inflammation to protect islet cells; and improving diabetes complications. In this review, we summarized the mechanisms by which cinnamon regulates CVDs and diabetes in order to provide a theoretical basis for the further clinical application of cinnamon.
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The role of the gut microbiome and its metabolites in metabolic diseases.
Wu, J, Wang, K, Wang, X, Pang, Y, Jiang, C
Protein & cell. 2021;(5):360-373
Abstract
It is well known that an unhealthy lifestyle is a major risk factor for metabolic diseases, while in recent years, accumulating evidence has demonstrated that the gut microbiome and its metabolites also play a crucial role in the onset and development of many metabolic diseases, including obesity, type 2 diabetes, nonalcoholic fatty liver disease, cardiovascular disease and so on. Numerous microorganisms dwell in the gastrointestinal tract, which is a key interface for energy acquisition and can metabolize dietary nutrients into many bioactive substances, thus acting as a link between the gut microbiome and its host. The gut microbiome is shaped by host genetics, immune responses and dietary factors. The metabolic and immune potential of the gut microbiome determines its significance in host health and diseases. Therefore, targeting the gut microbiome and relevant metabolic pathways would be effective therapeutic treatments for many metabolic diseases in the near future. This review will summarize information about the role of the gut microbiome in organism metabolism and the relationship between gut microbiome-derived metabolites and the pathogenesis of many metabolic diseases. Furthermore, recent advances in improving metabolic diseases by regulating the gut microbiome will be discussed.
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The Role of the Adipokine Leptin in Immune Cell Function in Health and Disease.
Kiernan, K, MacIver, NJ
Frontiers in immunology. 2020;:622468
Abstract
Leptin is a critical mediator of the immune response to changes in overall nutrition. Leptin is produced by adipocytes in proportion to adipose tissue mass and is therefore increased in obesity. Despite having a well-described role in regulating systemic metabolism and appetite, leptin displays pleiotropic actions, and it is now clear that leptin has a key role in influencing immune cell function. Indeed, many immune cells have been shown to respond to leptin directly via the leptin receptor, resulting in a largely pro-inflammatory phenotype. Understanding the role of adipose-tissue derived mediators in inflammation is critical to determining the pathophysiology of multiple obesity-associated diseases, such as type 2 diabetes, autoimmune disease, and infection. This review, therefore, focuses on the latest data regarding the role of leptin in modulating inflammation.
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The role of glucose homeostasis on immune function in response to exercise: The impact of low or higher energetic conditions.
Von Ah Morano, AE, Dorneles, GP, Peres, A, Lira, FS
Journal of cellular physiology. 2020;(4):3169-3188
Abstract
Immune cells are bioenergetically expensive during activation, which requires tightly regulated control of metabolic pathways. Both low and high glycemic conditions can modulate immune function. States of undernourishment depress the immune system, and in the same way, excessive intake of nutrients, such as an obesity state, compromise its functioning. Multicellular organisms depend on two mechanisms to survive: the regulation and ability to store energy to prevent starvation and the ability to fight against infection. Synergic interactions between metabolism and immunity affect many systems underpinning human health. In a chronic way, the breakdown of glycemic homeostasis in the body can influence cells of the immune system and consequently contribute to the onset of diseases such as type II diabetes, obesity, Alzheimer's, and fat and lean mass loss. On the contrary, exercise, recognized as a primary strategy to control hyperglycemic disorders, also induces a coordinated immune-neuro-endocrine response that acutely modulates cardiovascular, respiratory, and muscle functions and the immune response to exercise is widely dependent on the intensity and volume that may affect an immunodepressive state. These altered immune responses induced by exercise are modulated through the "stress hormones" adrenaline and cortisol, which are a threat to leukocyte metabolism. In this context, carbohydrates appear to have a positive acute response as a strategy to prevent depression of the immune system by maintaining plasma glucose concentrations to meet the energy demand from all systems involved during strenuous exercises. Therefore, herein, we discuss the mechanisms through which exercise may promotes changes on glycemic homeostasis in the metabolism and how it affects immune cell functions under higher or lower glucose conditions.
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Obesity Reduces mTORC1 Activity in Mucosal-Associated Invariant T Cells, Driving Defective Metabolic and Functional Responses.
O'Brien, A, Loftus, RM, Pisarska, MM, Tobin, LM, Bergin, R, Wood, NAW, Foley, C, Mat, A, Tinley, FC, Bannan, C, et al
Journal of immunology (Baltimore, Md. : 1950). 2019;(12):3404-3411
Abstract
Obesity underpins the development of numerous chronic diseases, such as type II diabetes mellitus. It is well established that obesity negatively alters immune cell frequencies and functions. Mucosal-associated invariant T (MAIT) cells are a population of innate T cells, which we have previously reported are dysregulated in obesity, with altered circulating and adipose tissue frequencies and a reduction in their IFN-γ production, which is a critical effector function of MAIT cells in host defense. Hence, there is increased urgency to characterize the key molecular mechanisms that drive MAIT cell effector functions and to identify those which are impaired in the obesity setting. In this study, we found that MAIT cells significantly upregulate their rates of glycolysis upon activation in an mTORC1-dependent manner, and this is essential for MAIT cell IFN-γ production. Furthermore, we show that mTORC1 activation is dependent on amino acid transport via SLC7A5. In obese patients, using RNA sequencing, Seahorse analysis, and a series of in vitro experiments, we demonstrate that MAIT cells isolated from obese adults display defective glycolytic metabolism, mTORC1 signaling, and SLC7A5 aa transport. Collectively, our data detail the intrinsic metabolic pathways controlling MAIT cell cytokine production and highlight mTORC1 as an important metabolic regulator that is impaired in obesity, leading to altered MAIT cell responses.