Browsing by Subject "hyperglycemia"

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    Hyperglycemia, symptoms, and symptom clusters in colorectal cancer survivors with type 2 diabetes
    (Springer, 2022-12) Storey, Susan; Luo, Xiao; Ofner, Susan; Perkins, Susan M.; Von Ah, Diane; School of Nursing
    Purpose The purpose of the study was to compare the individual and total number of symptoms and explore symptom clusters by hyperglycemia status in colorectal cancer survivors (CRCS) with diabetes (type 2). Methods A retrospective cohort study was conducted, whereby symptom data were extracted from clinical notes in electronic health records. CRCS (stage II or III) diagnosed between 2007 and 2017 who had diabetes and at least one HbA1c within 8 months of initial chemotherapy were included. Zero-inflated negative binomial regression analysis was used to examine total symptoms by hyperglycemia status (hyperglycemia versus no hyperglycemia). Exploratory factor analysis was conducted to identify symptom clusters. Results Two hundred forty-three CRCS met inclusion criteria. CRCS with hyperglycemia (HbA1c ≥ 6.5%) had greater individual symptoms (fatigue and depression) and total number of symptoms than those with no hyperglycemia. Two distinct symptom clusters, with five (nausea, vomiting, constipation, fatigue, and peripheral neuropathy) and two symptoms (anxiety and depression), were identified among CRCS with hyperglycemia. Conclusion These findings indicate that CRCS with diabetes and hyperglycemia had more symptoms and two distinct symptom clusters compared to those with no hyperglycemia. Prospective research studies are needed to examine the role of hyperglycemia in symptoms among CRCS with diabetes. Understanding hyperglycemia’s influence is important as it is a modifiable risk factor towards which prevention and intervention can be directed, potentially mitigating symptoms and symptom clusters and improving outcomes for CRCS with diabetes.
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    Insulin-inducible SMILE inhibits hepatic gluconeogenesis
    (ADA, 2016-11) Lee, Ji-Min; Seo, Woo-Young; Han, Hye-Sook; Oh, Kyoung-Jin; Lee, Yong-Soo; Kim, Don-Kyu; Choi, Seri; Choi, Byeong Hun; Harris, Robert A.; Lee, Chul-Ho; Koo, Seung-Hoi; Choi, Hueng-Sik; Department of Biochemistry & Molecular Biology, IU School of Medicine
    The role of a glucagon/cAMP-dependent protein kinase–inducible coactivator PGC-1α signaling pathway is well characterized in hepatic gluconeogenesis. However, an opposing protein kinase B (PKB)/Akt-inducible corepressor signaling pathway is unknown. A previous report has demonstrated that small heterodimer partner–interacting leucine zipper protein (SMILE) regulates the nuclear receptors and transcriptional factors that control hepatic gluconeogenesis. Here, we show that hepatic SMILE expression was induced by feeding in normal mice but not in db/db and high-fat diet (HFD)-fed mice. Interestingly, SMILE expression was induced by insulin in mouse primary hepatocyte and liver. Hepatic SMILE expression was not altered by refeeding in liver-specific insulin receptor knockout (LIRKO) or PKB β-deficient (PKBβ−/−) mice. At the molecular level, SMILE inhibited hepatocyte nuclear factor 4–mediated transcriptional activity via direct competition with PGC-1α. Moreover, ablation of SMILE augmented gluconeogenesis and increased blood glucose levels in mice. Conversely, overexpression of SMILE reduced hepatic gluconeogenic gene expression and ameliorated hyperglycemia and glucose intolerance in db/db and HFD-fed mice. Therefore, SMILE is an insulin-inducible corepressor that suppresses hepatic gluconeogenesis. Small molecules that enhance SMILE expression would have potential for treating hyperglycemia in diabetes.