Patient involvement in consultation for atrial fibrillation - the cardiologists' perspective.

PURPOSE: The purpose of this paper is to analyse the accounts of Swedish cardiologists concerning patient involvement in consultations for atrial fibrillation (AF). The questions were: how cardiologists handle and provide scope for patient involvement in medical consultations regarding AF treatment and how cardiologists describe their familiarity with shared decision-making. DESIGN/METHODOLOGY/APPROACH: A descriptive study was designed. Ten interviews with cardiologists at four Swedish hospitals were held, and a qualitative content analysis was performed on the collected data. FINDINGS: The analysis shows cardiologists' accounts of persuasive practice, protective practice, professional role and medical craftsmanship when it comes to patient involvement and shared decision-making. The term "shared decision-making" implies a concept of not only making one decision but also ensuring that it is finalised with a satisfactory agreement between both parties involved, the patient as well as the cardiologist. In order for the idea of patient involvement to be fulfilled, the two parties involved must have equal power, which can never actually be guaranteed. RESEARCH LIMITATIONS/IMPLICATIONS: Methodologically, this paper reflects the special contribution that can be made by the research design of descriptive qualitative content analysis (Krippendorff, 2004) to reveal and understand cardiologists' perspectives on patient involvement and participation in medical consultation and shared decision-making. The utility of this kind of analysis is to find what cardiologists said and how they arrived at their understanding about patient involvement. Accordingly, there is no quantification in this type of research. PRACTICAL IMPLICATIONS: Cardiologists should prioritise patient involvement and participation in decision-making regarding AF treatment decisions in consultations when trying to meet the request of patient involvement. ORIGINALITY/VALUE: Theoretically, the authors have learned that the patient involvement and shared decision-making requires the ability to see patients as active participants in the medical consultation process.

Effect of adipocyte-derived IGF-I on adipose tissue mass and glucose metabolism in the Berlin Fat Mouse.

Besides liver, IGF-I is expressed in adipose tissue. However, the effects of this local IGF-I on adipose tissue and metabolism are unclear. We generated adipocyte-specific knock-out mice on the background of the Berlin Fat Mouse Inbred (BFMI) line to evaluate the contribution of adipocyte-IGF-I on glucose metabolism and adipose tissue development. BFMI mice are obese, non-diabetic with elevated plasma insulin and IGF-I concentration. The knock-out in adipocytes led to a total white adipose tissue expression of 50-60% due to unaltered Igf-1 expression in stromavascular cells. The lack of IGF-I from adipocytes did not alter plasma IGF-I concentration. BFMIChr3-Igf-I-KOQ-AT mice had reduced adipose tissue mass in most depots. During oral glucose tolerance tests, BFMIChr3-Igf-I-KOQ-AT mice showed an impaired glucose clearance (p = .03). Interestingly, insulin action was enhanced during insulin tolerance tests (p = .05). In conclusion, adipocyte-specific IGF-I ablation in obese BFMI mice results in reduced adipose tissue mass and thereby alters glucose metabolism.

The direction of cross affects [corrected] obesity after puberty in male but not female offspring.

BACKGROUND: We investigated parent-of-origin and allele-specific expression effects on obesity and hepatic gene expression in reciprocal crosses between the Berlin Fat Mouse Inbred line (BFMI) and C57Bl/6NCrl (B6N). RESULTS: We found that F1-males with a BFMI mother developed 1.8 times more fat mass on a high fat diet at 10 weeks than F1-males of a BFMI father. The phenotype was detectable from six weeks on and was preserved after cross-fostering. RNA-seq data of liver provided evidence for higher biosynthesis and elongation of fatty acids (p = 0.00635) in obese male offspring of a BFMI mother versus lean offspring of a BFMI father. Furthermore, fatty acid degradation (p = 0.00198) and the peroxisome pathway were impaired (p = 0.00094). The circadian rhythm was affected as well (p = 0.00087). Among the highest up-regulated protein coding genes in obese males were Acot4 (1.82 fold, p = 0.022), Cyp4a10 (1.35 fold, p = 0.026) and Cyp4a14 (1.32 fold, p = 0.012), which hydroxylize fatty acids and which are known to be increased in liver steatosis. Obese males showed lower expression of the genetically imprinted and paternally expressed 3 (Peg3) gene (0.31 fold, p = 0.046) and higher expression of the androgen receptor (Ar) gene (2.38 fold, p = 0.068). Allelic imbalance was found for expression of ATP-binding cassette transporter gene Abca8b. Several of the differentially expressed genes contain estrogen response elements. CONCLUSIONS: Parent-of-origin effects during gametogenesis and/or fetal development in an obese mother epigenetically modify the transcription of genes that lead to enhanced fatty acid synthesis and impair ß-oxidation in the liver of male, but not female F1 offspring. Down-regulation of Peg3 could contribute to trigger this metabolic setting. At puberty, higher amounts of the androgen receptor and altered access to estrogen response elements in affected genes are likely responsible for male specific expression of genes that were epigenetically triggered. A suggestive lack of estrogen binding motifs was found for highly down-regulated genes in adult hepatocytes of obese F1 males (p = 0.074).