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Browsing by Subject "Adipose Tissue"

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    Binding of insulin with adipose cells and with lecithin
    (1966) Tan, Wee-Chong
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    Bone marrow fat is increased in chronic kidney disease by magnetic resonance spectroscopy
    (Springer-Verlag, 2015-06) Moorthi, R. N.; Fadel, W.; Eckert, G. J.; Ponsler-Sipes, K.; Moe, S. M.; Lin, C.; Department of Medicine, IU School of Medicine
    In aging, the bone marrow fills with fat and this may lead to higher fracture risk. We show that a bone marrow fat measurement by magnetic resonance spectroscopy (MRS), a newer technique not previously studied in chronic kidney disease (CKD), is useful and reproducible. CKD patients have significantly higher bone marrow fat than healthy adults. INTRODUCTION: Renal osteodystrophy leads to increased morbidity and mortality in patients with CKD. Traditional bone biopsy histomorphometry is used to study abnormalities in CKD, but the bone marrow, the source of osteoblasts, has not been well characterized in patients with CKD. METHODS: To determine the repeatability of bone marrow fat fraction assessment by MRS and water-fat imaging (WFI) at four sites in patients with CKD, testing was performed to determine the coefficients of reproducibility and intraclass coefficients (ICCs). We further determined if this noninvasive technique could be used to determine if there are differences in the percent bone marrow fat in patients with CKD compared to matched controls using paired t tests. RESULTS: The mean age of subjects with CKD was 59.8 ± 7.2 years, and the mean eGFR was 24 ± 8 ml/min. MRS showed good reproducibility at all sites in subjects with CKD and controls, with a coefficient of reproducibilities ranging from 2.4 to 13 %. MRS and WFI assessment of bone marrow fat showed moderate to strong agreement (ICC 0.6-0.7) at the lumbar spine, with poorer agreement at the iliac crest and no agreement at the tibia. The mean percent bone marrow fat at L2-L4 was 13.8 % (95 % CI 8.3-19.7) higher in CKD versus controls (p < 0.05). CONCLUSIONS: MRS is a useful and reproducible technique to study bone marrow fat in CKD. Patients with CKD have significantly higher bone marrow fat than healthy adults; the relationship with bone changes requires further analyses.
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    Consumption of Diet Soda Sweetened with Sucralose and Acesulfame‐Potassium Alters Inflammatory Transcriptome Pathways in Females with Overweight and Obesity
    (Wiley, 2020-06) Sylvetsky, Allison C.; Sen, Sabyasachi; Merkel, Patrick; Dore, Fiona; Stern, David B.; Henry, Curtis J.; Cai, Hongyi; Walter, Peter J.; Crandall, Keith A.; Rother, Kristina I.; Hubal, Monica J.; Kinesiology, School of Health and Human Sciences
    SCOPE: Low-calorie sweetener (LCS) consumption is associated with metabolic disease in observational studies. However, physiologic mechanisms underlying LCS-induced metabolic impairments in humans are unclear. This study is aimed at identifying molecular pathways in adipose impacted by LCSs. METHODS AND RESULTS: Seven females with overweight or obesity, who did not report LCS use, consumed 12 ounces of diet soda containing sucralose and acesulfame-potassium (Ace-K) three times daily for 8 weeks. A subcutaneous adipose biopsy from the left abdomen and a fasting blood sample were collected at baseline and post-intervention. Global gene expression were assessed using RNA-sequencing followed by functional pathway analysis. No differences in circulating metabolic or inflammatory biomarkers were observed. However, ANOVA detected 828 differentially expressed annotated genes after diet soda consumption (p < 0.05), including transcripts for inflammatory cytokines. Fifty-eight of 140 canonical pathways represented in pathway analyses regulated inflammation, and several key upstream regulators of inflammation (e.g., TNF-alpha) were also represented. CONCLUSION: Consumption of diet soda with sucralose and Ace-K alters inflammatory transcriptomic pathways (e.g., NF-κB signaling) in subcutaneous adipose tissue but does not significantly alter circulating biomarkers. Findings highlight the need to examine molecular and metabolic effects of LCS exposure in a larger randomized control trial for a longer duration.
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    The effect of age on hormonal-regulation of lipolysis in isolated adipocytes of the rat
    (1972) Miller, Elizabeth Anne
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    Increasing serum pre-adipocyte factor-1 (Pref-1) correlates with decreased body fat, increased free fatty acids, and level of recent alcohol consumption in excessive alcohol drinkers
    (Elsevier, 2014-12) Liangpunsakul, Suthat; Bennett, Rachel; Westerhold, Chi; Ross, Ruth A.; Crabb, David W.; Lai, Xianyin; Witzmann, Frank A.; Department of Medicine, IU School of Medicine
    Patients with alcoholic liver disease have been reported to have a significantly lower percentage of body fat (%BF) than controls. The mechanism for the reduction in %BF in heavy alcohol users has not been elucidated. In adipose tissue, Pref-1 is specifically expressed in pre-adipocytes but not in adipocytes. Pref-1 inhibits adipogenesis and elevated levels are associated with reduced adipose tissue mass. We investigated the association between serum Pref-1 and %BF, alcohol consumption, and serum free fatty acids (FFA) in a well-characterized cohort of heavy alcohol users compared to controls. One hundred forty-eight subjects were prospectively recruited. The Time Line Follow-Back (TLFB) questionnaire was used to quantify the amount of alcohol consumed over the 30-day period before their enrollment. Anthropometric measurements were performed to calculate %BF. Serum Pref-1 and FFA were measured. Fifty-one subjects (mean age 32 ± 9 years, 88% men) were non-excessive drinkers whereas 97 were excessive drinkers (mean age 41 ± 18 years, 69% men). Compared to non-excessive drinkers, individuals with excessive drinking had significantly higher levels of Pref-1 (p<0.01), FFA (p < 0.001), and lower %BF (p = 0.03). Serum levels of Pref-1 were associated with the amount of alcohol consumed during the previous 30 days. Serum Pref-1 was negatively correlated with %BF, but positively associated with serum FFA. Our data suggest that elevated Pref-1 levels in excessive drinkers might inhibit the expansion of adipose tissue, decreasing %BF in alcoholics. Further work is needed to validate these findings and to better understand the role of Pref-1 and its clinical significance in subjects with heavy alcohol use.
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    Key Role of STAT4 Deficiency in the Hematopoietic Compartment in Insulin Resistance and Adipose Tissue Inflammation
    (Hindawi Publishing Corporation, 2017) Dobrian, Anca D.; Ma, Kaiwen; Glenn, Lindsey M.; Hatcher, Margaret A.; Haynes, Bronson A.; Lehrer, Eric J.; Kaplan, Mark H.; Nadler, Jerry L.; Pediatrics, School of Medicine
    Dobrian, A. D., Ma, K., Glenn, L. M., Hatcher, M. A., Haynes, B. A., Lehrer, E. J., … Nadler, J. L. (2017). Key Role of STAT4 Deficiency in the Hematopoietic Compartment in Insulin Resistance and Adipose Tissue Inflammation. Mediators of Inflammation, 2017, 5420718. http://doi.org/10.1155/2017/5420718
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    Lean and Obese Coronary Perivascular Adipose Tissue Impairs Vasodilation via Differential Inhibition of Vascular Smooth Muscle K+ Channels
    (Ovid Technologies Wolters Kluwer - American Heart Association, 2015-06) Noblet, Jillian N.; Owen, Meredith K.; Goodwill, Adam G.; Sassoon, Daniel J.; Tune, Johnathan D.; Department of Cellular & Integrative Physiology, IU School of Medicine
    OBJECTIVE: The effects of coronary perivascular adipose tissue (PVAT) on vasomotor tone are influenced by an obese phenotype and are distinct from other adipose tissue depots. The purpose of this investigation was to examine the effects of lean and obese coronary PVAT on end-effector mechanisms of coronary vasodilation and to identify potential factors involved. APPROACH AND RESULTS: Hematoxylin and eosin staining revealed similarities in coronary perivascular adipocyte size between lean and obese Ossabaw swine. Isometric tension studies of isolated coronary arteries from Ossabaw swine revealed that factors derived from lean and obese coronary PVAT attenuated vasodilation to adenosine. Lean coronary PVAT inhibited K(Ca) and KV7, but not KATP channel-mediated dilation in lean arteries. In the absence of PVAT, vasodilation to K(Ca) and KV7 channel activation was impaired in obese arteries relative to lean arteries. Obese PVAT had no effect on K(Ca) or KV7 channel-mediated dilation in obese arteries. In contrast, obese PVAT inhibited KATP channel-mediated dilation in both lean and obese arteries. The differential effects of obese versus lean PVAT were not associated with changes in either coronary KV7 or K(ATP) channel expression. Incubation with calpastatin attenuated coronary vasodilation to adenosine in lean but not in obese arteries. CONCLUSIONS: These findings indicate that lean and obese coronary PVAT attenuates vasodilation via inhibitory effects on vascular smooth muscle K(+) channels and that alterations in specific factors such as calpastatin are capable of contributing to the initiation or progression of smooth muscle dysfunction in obesity.
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    Lipid mobilization in adipose tissue
    (1963) Carr, Lucinda Gayle
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    Lipodermoid Cyst: A Report of a Rare Caruncular Case
    (Medknow Publications, 2015-10) Rajabi, Mohammad Taher; Ramezani, Koosha; Department of Ophthalmology, IU School of Medicine
    Ocular lipodermoid cysts and solid dermoid tumors are choristomas which are described as normal tissue growth in an abnormal location. Congenital epibulbar lipodermoid comprises adipose tissue that is covered by connective tissue. They are usually located superotemporally, and basically tend not to involve the peripheral cornea. If the dermoid or lipodermoid is accompanied by other systemic conditions or ocular anomalies in young children, a consultation with an Internist or pediatrician is required to rule out Goldenhar syndrome which is a oculoauriculovertebral dysplasia. This paper reports a unilateral lipodermoid cyst which is remarkable regarding its caruncular origin, in an otherwise healthy adult female.
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    Mechanisms for the effects of adipose tissue-derived stromal/stem cells on angiogenesis and tissue repair in schemic diseases
    (2008) Cai, Liying
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