The influence of intermittent hypoxia, obesity and diabetes on male genitourinary anatomy and voiding physiology

2021 ◽  
Author(s):  
Lisa L Abler ◽  
Chelsea A O'Driscoll ◽  
Sara A Colopy ◽  
Kimberly P Keil Stietz ◽  
Peiqing Wang ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Intermittent Hypoxia ◽  
Dark Period ◽  
Relative Weight ◽  
Mutant Mice ◽  
Wild Type ◽  
Anatomy And Physiology ◽  
Obesity And Diabetes ◽  
Specific Manifestation

We used male BTBR mice carrying the Lepob mutation, which are subject to severe and progressive obesity and diabetes beginning at 6 weeks of age, to examine the influence of one specific manifestation of sleep apnea, intermittent hypoxia, on male urinary voiding physiology and genitourinary anatomy. A custom device was used to deliver continuous normoxia (NX, control) or intermittent hypoxia (IH) to wild type and Lepob/ob (mutant) mice for 2 weeks. Intermittent hypoxia was delivered during the 12-hour inactive (lighted) period in the form of 90 sec of 6% O2 followed by 90 sec of room air. Continuous room air was delivered during the 12-hour active (dark) period. We then evaluated genitourinary anatomy and physiology. As expected for the type 2 diabetes phenotype, mutant mice consume more food and water, weighed more, and voided more frequently and in larger urine volumes. They also have larger bladder volumes but smaller prostates, seminal vesicles, and urethras than wild type mice. IH decreases food consumption and increases bladder relative weight independent of genotype and increases urine glucose concentration in mutant mice. When evaluated based on genotype (NX+IH), the incidence of pathogenic bacteriuria is greater in mutant than wild type mice, and among mice exposed to IH, bacteriuria incidence is greater in mutant than wild type mice. We conclude that IH exposure and type 2 diabetes can act independently and together to modify male mouse urinary function.

The Role of Physical Exercise in Obesity and Diabetes

2018 ◽  
Vol 66 (3) ◽  
Keyword(s):  
Type 2 Diabetes ◽  
Type 1 Diabetes ◽  
Glycemic Control ◽  
Physical Exercise ◽  
Treatment Guidelines ◽  
Treatment Guideline ◽  
Obesity And Diabetes ◽  
Regular Physical Exercise

The prevalence of obesity is increasing world-wide. Obesity is associated with a plethora of metabolic and clinical constraints, which result in a higher risk for the development of cardiovascular complications and metabolic disease, particularly insulin resistance and type 2 diabetes. Obesity is an acknowledged determinant of glycemic control in patients with type 1 diabetes and accounts for the majority of premature death due to cardiovascular events. Physical exercise is generally recommended in patients with diabetes in order to prevent the development of or reduce existing obesity, as adopted by every international treatment guideline so far. Regular physical exercise has a beneficial impact on body composition, cardiovascular integrity, insulin sensitivity and quality of life. However, only a minority of patients participates in regular physical exercise, due to individual or ­disease-related barriers. In type 2 diabetes, there is robust evidence for beneficial effects of physical exercise on glycemic control, cardiovascular health and the development of diabetes-related long-term complications. In type 1 diabetes and patients treated with insulin, a higher risk for exercise-­related hypoglycemia has to be considered, which requires certain prerequisites and adequate adaptions of insulin ­dosing. Current treatment guidelines do only incompletely address the development of exercise-related hypoglycemia. However, every patient with diabetes should participate in regular physical exercise in order to support and enable ­sufficient treatment and optimal glycemic control.

Immunometabolism of obesity and diabetes: microbiota link compartmentalized immunity in the gut to metabolic tissue inflammation

2015 ◽  
Vol 129 (12) ◽  
pp. 1083-1096 ◽  
Author(s):  
Joseph B. McPhee ◽  
Jonathan D. Schertzer
Keyword(s):  
Metabolic Disease ◽  
Type 2 Diabetes ◽  
Immune Responses ◽  
Metabolic Diseases ◽  
The Body ◽  
Tissue Inflammation ◽  
Gut Barrier Function ◽  
Inflammatory Status ◽  
Obesity And Diabetes

The bacteria that inhabit us have emerged as factors linking immunity and metabolism. Changes in our microbiota can modify obesity and the immune underpinnings of metabolic diseases such as Type 2 diabetes. Obesity coincides with a low-level systemic inflammation, which also manifests within metabolic tissues such as adipose tissue and liver. This metabolic inflammation can promote insulin resistance and dysglycaemia. However, the obesity and metabolic disease-related immune responses that are compartmentalized in the intestinal environment do not necessarily parallel the inflammatory status of metabolic tissues that control blood glucose. In fact, a permissive immune environment in the gut can exacerbate metabolic tissue inflammation. Unravelling these discordant immune responses in different parts of the body and establishing a connection between nutrients, immunity and the microbiota in the gut is a complex challenge. Recent evidence positions the relationship between host gut barrier function, intestinal T cell responses and specific microbes at the crossroads of obesity and inflammation in metabolic disease. A key problem to be addressed is understanding how metabolite, immune or bacterial signals from the gut are relayed and transferred into systemic or metabolic tissue inflammation that can impair insulin action preceding Type 2 diabetes.

scholarly journals Quinoa’s Potential to Enhance Dietary Management of Obesity and Type-2 Diabetes: A Review of the Current Evidence

Diabetology ◽  
2021 ◽  
Vol 2 (2) ◽  
pp. 77-94
Author(s):  
Alexander Little ◽  
Kevin Murphy ◽  
Patrick Solverson
Keyword(s):  
Type 2 Diabetes ◽  
Best Management Practices ◽  
Management Practices ◽  
The United States ◽  
Lipid Absorption ◽  
Current Evidence ◽  
Future Research ◽  
Dietary Management ◽  
Obesity And Diabetes

The prevalence of diet-induced obesity and type-2 diabetes remains a growing concern in the United States. As best management practices still include improved diet and physical activity, bioactive food components, contained within functional foods, show promise in curbing the cardiometabolic complications associated with excess weight and diabetes. Quinoa is an emerging candidate crop for its versatility in wide-ranging growing conditions as one approach to address food security, but it also contains several components that may serve as a dietary tool for post-industrial countries struggling with the health complications of caloric excess. Preliminary rodent feeding studies demonstrate that components within quinoa, namely, phytosteroids, phenolics, polysaccharides, and peptides, can prevent adiposity, dyslipidemia, and hyperglycemia. Mechanistic activity may involve reduced lipid absorption and adipogenesis, increased energy expenditure and glucose oxidation and corrected gut microbiota. Other intestinal actions may include blocked carbohydrate digestion with enhanced incretin signaling. Evidence in clinical trials is lacking and future research spanning cells to the clinic is needed to further elucidate the interesting preliminary reports reviewed here. Quinoa offers several unique attributes that could be harnessed to improve the dietary management of obesity and diabetes.

Mutation of the 5' untranslated region stem-loop mRNA structure reduces type I collagen deposition and arterial stiffness in male obese mice

2021 ◽  
Author(s):  
Francisco I. Ramirez-Perez ◽  
Makenzie L. Woodford ◽  
Mariana Morales-Quinones ◽  
Zachary I. Grunewald ◽  
Francisco J Cabral-Amador ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Arterial Stiffness ◽  
Type I Collagen ◽  
Type I ◽  
Collagen Deposition ◽  
Wild Type ◽  
Stem Loop ◽  
Arterial Stiffening

Arterial stiffening, a characteristic feature of obesity and type 2 diabetes, contributes to the development and progression of cardiovascular diseases (CVD). Currently, no effective prophylaxis or therapeutics is available to prevent or treat arterial stiffening. A better understanding of the molecular mechanisms underlying arterial stiffening is vital to identify newer targets and strategies to reduce CVD burden. A major contributor to arterial stiffening is increased collagen deposition. In the 5' untranslated regions of mRNAs encoding for type I collagen, an evolutionally conserved stem-loop (SL) structure plays an essential role in its stability and post-transcriptional regulation. Here, we show that feeding a high fat/high sucrose (HFHS) diet for 28 weeks increases adiposity, insulin resistance, and blood pressure in male wild-type littermates. Moreover, arterial stiffness, assessed in vivo via aortic pulse wave velocity, and ex vivo using atomic force microscopy in aortic explants or pressure myography in isolated femoral and mesenteric arteries, was also increased in those mice. Notably, all these indices of arterial stiffness, along with collagen type I levels in the vasculature, were reduced in HFHS-fed mice harboring a mutation in the 5'SL structure, relative to wild-type littermates. This protective vascular phenotype in 5'SL-mutant mice did not associate with a reduction in insulin resistance or blood pressure. These findings implicate the 5'SL structure as a putative therapeutic target to prevent or reverse arterial stiffening and CVD associated with obesity and type 2 diabetes.

LDL receptor but not apolipoprotein E deficiency increases diet-induced obesity and diabetes in mice

2002 ◽  
Vol 282 (1) ◽  
pp. E207-E214 ◽  
Author(s):  
Sandra A. Schreyer ◽  
Cynthia Vick ◽  
Theodore C. Lystig ◽  
Paul Mystkowski ◽  
Renée C. LeBoeuf
Keyword(s):  
Apolipoprotein E ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Wild Type ◽  
Glucose Levels ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes ◽  
Glucose And Lipid Homeostasis

The aim of this study was to determine whether phenotypes associated with type 2 diabetes are altered in dyslipidemic obese mice. C57BL/6 wild-type, low-density lipoprotein (LDL) receptor-deficient (LDLR−/−), and apolipoprotein E-deficient (apoE−/−) mice were fed a high-fat, high-carbohydrate diet (diabetogenic diet), and the development of obesity, diabetes, and hypertriglyceridemia was examined. Wild-type mice became obese and developed hyperglycemia, but not hypertriglyceridemia, in response to this diet. LDLR−/− mice fed the diabetogenic diet became more obese than wild-type mice and developed severe hypertriglyceridemia and hyperleptinemia. Surprisingly, glucose levels were only modestly higher and insulin levels and insulin-to-glucose ratios were not strikingly different from those of wild-type mice. In contrast, diabetogenic diet-fed apoE−/− mice were resistant to changes in glucose and lipid homeostasis despite becoming obese. These data suggest that modifications in lipoprotein profiles associated with loss of the LDL receptor or apoE function have profound and unique consequences on susceptibility to diet-induced obesity and type 2 diabetic phenotypes.

scholarly journals Role of folate in nonalcoholic fatty liver disease

2017 ◽  
Vol 95 (10) ◽  
pp. 1141-1148 ◽  
Author(s):  
Victoria Sid ◽  
Yaw L. Siow ◽  
Karmin O
Keyword(s):  
Type 2 Diabetes ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Serum Folate ◽  
Nonalcoholic Fatty Liver ◽  
Obesity And Diabetes

Nonalcoholic fatty liver disease (NAFLD) is a spectrum of chronic liver conditions that are characterized by steatosis, inflammation, fibrosis, and liver injury. The global prevalence of NAFLD is rapidly increasing in proportion to the rising incidence of obesity and type 2 diabetes. Because NAFLD is a multifaceted disorder with many underlying metabolic abnormalities, currently, there is no pharmacological agent that is therapeutically approved for the treatment of this disease. Folate is a water-soluble B vitamin that plays an essential role in one-carbon transfer reactions involved in nucleic acid biosynthesis, methylation reactions, and sulfur-containing amino acid metabolism. The liver is the primary organ responsible for storage and metabolism of folates. Low serum folate levels have been observed in patients with obesity and diabetes. It has been reported that a low level of endogenous folates in rodents perturbs folate-dependent one-carbon metabolism, and may be associated with development of metabolic diseases such as NAFLD. This review highlights the biological role of folate in the progression of NAFLD and its associated metabolic complications including obesity and type 2 diabetes. Understanding the role of folate in metabolic disease may position this vitamin as a potential therapeutic for NAFLD.

scholarly journals Gestational microbiome: metabolic perturbations and developmental programming

Reproduction ◽  
2021 ◽  
Vol 162 (6) ◽  
pp. R85-R98
Author(s):  
Sophia Han ◽  
Charlotte C Ellberg ◽  
Isoken N Olomu ◽  
Arpita K Vyas
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Human Microbiome ◽  
Disease States ◽  
Microbial Dysbiosis ◽  
Obesity And Diabetes ◽  
Growing Body

A growing body of research suggests that alterations to the human microbiome are associated with disease states, including obesity and diabetes. During pregnancy, these disease states are associated with maternal microbial dysbiosis. This review discusses the current literature regarding the typical maternal and offspring microbiome as well as alterations to the microbiome in the context of obesity, type 2 diabetes mellitus, and gestational diabetes mellitus. Furthermore, this review outlines the proposed mechanisms linking associations between the maternal microbiome in the aforementioned disease states and offspring microbiome. Additionally, this review highlights associations between alterations in offspring microbiome and postnatal health outcomes.

scholarly journals Association of Bariatric Surgery With Cancer Incidence in Patients With Obesity and Diabetes: Long-term Results From the Swedish Obese Subjects Study

2021 ◽  
Author(s):  
Kajsa Sjöholm ◽  
Lena MS Carlsson ◽  
Per-Arne Svensson ◽  
Johanna C. Andersson-Assarsson ◽  
Felipe Kristensson ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Bariatric Surgery ◽  
Cancer Risk ◽  
Cancer Incidence ◽  
Diabetes Remission ◽  
Obesity And Diabetes ◽  
Obese Subjects

<b>OBJECTIVE</b> <p>Obesity and type 2 diabetes are associated with serious, adverse health effects, including cancer. Although bariatric surgery has been shown to reduce cancer risk in patients with obesity, the effect of bariatric surgery on cancer risk in patients with obesity and diabetes is less studied. We therefore examined the long-term incidence of cancer after bariatric surgery and usual care in patients with obesity and diabetes in the matched prospective Swedish Obese Subjects (SOS) study. </p> <p><b>RESEARCH DESIGN AND METHODS</b></p> <p>The SOS study examines long-term outcomes following bariatric surgery or usual care. The current analysis includes 701 patients with obesity and type 2 diabetes at baseline, 393 of which underwent bariatric surgery, and 308 who received conventional obesity treatment. Information on cancer events was obtained from the Swedish National Cancer Register. Median follow-up time was 21.3 years (interquartile range 17.6-24.8 years, maximum 30.7 years). </p> <p><b>RESULTS</b></p> <p>During follow-up, the incidence rate for first-time cancer was 9.1 per 1000-person-years (95% CI, 7.2-11.5) in patients with obesity and diabetes treated with bariatric surgery and 14.1 per 1000-person-years (95% CI, 11.2-17.7) in patients treated with usual obesity care (HRadj=0.63; 95% CI 0.44-0.89, p=0.008). Moreover, surgery was associated with reduced cancer incidence in women (HRadj=0.58; 0.38-0.90, p=0.016), although the sex-treatment interaction was non-significant (p=0.630). In addition, diabetes remission at the 10-year follow-up was associated with reduced cancer incidence (HRadj=0.40; 95% CI 0.22-0.74, p=0.003).</p> <p><b>CONCLUSIONS</b></p> <p>These results suggest that bariatric surgery prevents cancer in patients with obesity and diabetes, and that durable diabetes remission is associated with reduced cancer risk. </p>

scholarly journals Docking protein 1 and free fatty acids are associated with insulin resistance in patients with type 2 diabetes mellitus

2021 ◽  
Vol 49 (11) ◽  
pp. 030006052110482
Author(s):  
Xiaoqin Ha ◽  
Xiaoling Cai ◽  
Huizhe Cao ◽  
Jie Li ◽  
Bo Yang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Effective Means ◽  
Model Assessment ◽  
High Concentration ◽  
Obesity And Diabetes ◽  
Docking Protein

Objective Insulin resistance (IR) is a key defect in type 2 diabetes mellitus (T2DM); therefore, effective means of ameliorating IR are sought. Methods We performed a retrospective cohort study of 154 patients with T2DM and 39 with pre-diabetes (pre-DM). The effects of IR and a high concentration of FFA on gene expression were determined using microarray analysis and quantitative reverse transcription polymerase chain reaction (RT-qPCR) in patients with T2DM or pre-DM. Results Serum FFA concentration and homeostasis model assessment of IR (HOMA-IR) were significantly higher in patients with T2DM but no obesity and in those with pre-DM than in controls. HOMA-IR was significantly associated with T2DM. RT-qPCR showed that the expression of FBJ murine osteosarcoma viral oncogene homolog ( FOS) and AE binding protein 1 ( AEBP1) was much lower in the circulation of participants with obesity and diabetes. RT-qPCR showed that the expression of docking protein 1 ( DOK1) was significantly lower in the blood of participants with diabetes but no obesity and in those with pre-DM than in controls. Conclusions FFA and DOK1 are associated with IR in patients with T2DM but no obesity or pre-DM. The downregulation of DOK1 might inhibit lipid synthesis and induce lipolysis, inducing or worsening IR.

scholarly journals BSMI AND TAQI POLYMORPHISMS IN VITAMIN D RECEPTOR GENE OF TYPE 2 DIABETES MELLITUS PATIENTS FROM NORTH INDIA

2016 ◽  
Vol 9 (9) ◽  
pp. 186 ◽  
Author(s):  
Nancy Taneja ◽  
Rajesh Khadagawat ◽  
Shalini Mani
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Vitamin D ◽  
Vitamin D Receptor ◽  
Metabolic Diseases ◽  
Fragment Length Polymorphism ◽  
Wild Type ◽  
Significant Difference ◽  
Restriction Fragment Length

ABSTRACTObjective: Polymorphisms in vitamin D receptor (VDR) genes are known to be linked with different metabolic diseases including Type 2 diabetesmellitus (T2DM) also. However, the association of these polymorphisms is not much explored for the Indian population. To determine the prevalenceof BsmI and TaqI polymorphism in VDR gene of T2DM patients from North India.Methods: Blood samples were obtained from 100 well-characterized T2DM patients and 100 healthy controls. Genomic DNA was isolated from bloodsamples and using polymerase chain reaction/restriction fragment length polymorphism based method, the presence of these polymorphisms wasinvestigated in these samples. The data were statistically analyzed using SPSS 21.0 software.Results: For TaqI polymorphism, both the wild type (TT) and heterozygous (TC) genotype showed a significant difference between patients andcontrols (p=0.023 and p<0.001, respectively). Whereas, the frequency of CC genotype was not significantly different among these groups (p=0.506).For BsmI polymorphism also, the frequency of wild type (GG) and heterozygous (GA) genotype was significantly different in patients and controls(p=0.027 and p=0.001), respectively. However, the frequency of AA genotype was not of statistical significance in patients (p=0.071).Conclusions: The mutant alleles of TaqI and BsmI polymorphisms are known to be associated with different metabolic diseases, including diabetestoo. In our study also, there is a significant difference between the frequency of wild type and heterozygous genotype for these polymorphisms. Thissuggests that BsmI and TaqI polymorphisms may be associated with T2DM patients.Keywords: Type 2 diabetes mellitus, Polymorphism, Vitamin D receptor, Patient, Control, Restriction fragment length polymorphism.

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