ABSTRACT
During educational dissection of cadavers, we encountered anatomical variability of the left phrenic nerve (PN). In this cadaver, nerve fibres from C3 and C4 descended and crossed behind the transverse cervical artery (TCA), a branch of the thyrocervical trunk, at the level of the anterior scalene muscle. On the other hand, nerve fibres from C5 descended obliquely above the TCA and then joined the fibres from C3-C4 on the medial side of the anterior scalene muscle to form the PN. To our knowledge, the encircling of the TCA by the left PN in the neck has not yet been reported and may pose a potential risk for nerve compression during movement of the neck. We discuss several types of anatomical variants of the PN and the associated risk during thorax and neck dissection procedures.
Subject(s)
Neck , Phrenic Nerve , Cadaver , Dissection , Humans , Phrenic Nerve/anatomy & histology , Subclavian ArteryABSTRACT
Leptin is an adipocyte-secreted hormone that binds hypothalamic receptors and potently decreases food intake. Leptin receptor defects in homozygous mutant Zucker fatty ( fa/fa) rats lead to massive obesity, hyperphagia, decreased energy expenditure, and insulin resistance, while the phenotype of heterozygous ( Fa/fa) lean rats lies between lean ( Fa/Fa) and obese ( fa/fa) rats. Whether heterezygotes exhibit specific changes in lipid metabolism in a diet-responsive manner is not clear. Thus, the specific aim of this study was to test whether the presence of one fa allele modulates lipid metabolism and leptin, and whether these effects are exacerbated by high-fat diet. We demonstrate that the presence of one fa allele significantly increases lipogenesis in adipose tissue assessed by glycerol-3-phosphate dehydrogenase (GPDH) and fatty acid synthase (FAS) activities. FAS is more responsive to high-fat diets than GPDH in Fa/fa rats. Adipose tissue leptin levels are significantly higher in fat pads of Fa/fa compared to Fa/Fa rats. Moreover, Fa/fa rats fed high-fat diet show an additional two-fold increase in leptin levels compared to wild type rats on the same diet. Collectively, these results indicate that the presence of one fa allele increase adipocyte lipogenic enzyme activities, which results in hyperleptinemia concurrent with increased adiposity.
Subject(s)
Adipose Tissue/metabolism , Dietary Fats/metabolism , Leptin/metabolism , Lipid Metabolism , Receptors, Cell Surface/genetics , Adipocytes/metabolism , Animals , Energy Metabolism/genetics , Fatty Acid Synthases/metabolism , Gene Expression , Glycerolphosphate Dehydrogenase/metabolism , Heterozygote , Liver/metabolism , Male , Rats , Rats, Mutant Strains , Rats, Zucker , Receptors, Cytokine/genetics , Receptors, LeptinABSTRACT
To address the role of angiotensinogen (agt) in lipid metabolism and its potential endocrine effects in vivo, we studied the effects of high-fat diet (HFD) on adult, 28-week-old agt knockout (KO) mice compared to wild type (WT) mice. Recent studies (Massiera et al., 2001) have demonstrated that reexpression of agt in adipose tissue of KO mice normalized adiposity, blood pressure, and kidney abnormalities. We therefore used microarray analysis to investigate changes in gene expression profile in kidneys of KO vs. Tg-KO mice, where agt expression is restricted to adipose tissue. Body weight, adiposity and insulin levels were significantly decreased (p < 0.05) in KO mice on a chow diet (CD) compared to WT mice, while circulating leptin levels were similar. On a high-fat diet, KO mice exhibited significantly lower bodyweight (p < 0.05), adiposity (p < 0.05), leptin, and insulin levels (p < 0.05) compared to WT mice. In agreement with previously reported changes in kidney histology, agt KO mice displayed altered expressions of genes involved in blood pressure regulation and renal function, but these levels were corrected by reexpression of agt in adipose tissue. Collectively, these findings further document important endocrine roles of adipocyte agt, in part via regulation of lipid metabolism and kidney homeostasis.
Subject(s)
Adipose Tissue/metabolism , Angiotensinogen/genetics , Angiotensinogen/metabolism , Dietary Fats/metabolism , Kidney/physiology , Lipid Metabolism , Angiotensinogen/deficiency , Animals , Blood Pressure/physiology , Body Composition/genetics , Body Weight/genetics , Gene Expression Profiling , Insulin/blood , Leptin/blood , Male , Mice , Mice, Knockout , Mice, Transgenic , Oligonucleotide Array Sequence AnalysisABSTRACT
This study investigated the effects of L-carnitine on insulin-like growth factor-I/II (IGF-I/II) and insulin-like growth factor binding proteins (IGFBPs) in streptozotocin (STZ)-induced diabetic rats. Each rat in the three L-carnitine-treated groups was injected subcutaneously with L-carnitine, 50 (D50), 100 (D100), or 200 (D200) mg/kg body weight every other day for four weeks, and animals in normal (N) and diabetic (DM) groups received saline by the same method. Diabetic rats had significantly lower carnitine concentrations in serum and liver compared with normal rats. Total carnitine concentrations were increased dose-dependently by carnitine treatment. Total IGF-I in serum from diabetic rats was increased dose-dependently by carnitine treatment, but was statistically significant only in the D200 group. The expression of liver IGF-I mRNA was lower in diabetic rats than in normal rats and increased by L-carnitine treatment. L-Carnitine treatment of diabetic rats had no effect on the levels of IGF-II in serum, liver, and kidney. Although the levels of IGF-II in serum and kidney of diabetic rats were increased in comparison with normal rats, IGF-II mRNA was not expressed in liver. Diabetic rats had markedly lower IGFBP-3 than normal rats did, and IGFBP-3 was increased by L-carnitine treatment. These results demonstrate that L-carnitine treatment of diabetic rats modulates the IGFs/IGFBPs axis. Especially note-worthy is that L-carnitine at a dose of 200 mg/kg/48 h for four weeks was able to restore serum total IGF-I in STZ-induced diabetic rats to nearly normal levels.
