The chemistry of death--Adipocere degradation in modern graveyards.

The formation of adipocere slows further decomposition and preserves corpses for decades or even centuries. This resistance to degradation is a serious problem, especially with regard to the reuse of graves after regular resting times. We present results from an exhumation series in modern graveyards where coffins from water-saturated earth graves contained adipocere embedded in black humic material after resting times of about 30 years. Based on the assumption that this humic material resulted from in situ degradation of adipocere, its presence contradicts the commonly held opinion that adipocere decomposition only occurs under aerobic conditions. To test our hypothesis, we collected black humic material, adipocere as well as soil samples above and below coffins from representative graves (n=7). A comprehensive chemical analysis of the samples substantiated our in situ degradation theory. Element compositions and fatty acid mass spectra confirmed that the humic black material originated from the corpses. A van Krevelen diagram classified the excavated adipocere material as lipid, whereas the black humic material was closer to the carbohydrate region. Mass fragmentograms of the humic material revealed the presence of large amounts of saturated vs. unsaturated nC16 and nC18 fatty acids, which is typical for adipocere. In addition, the soil samples exhibited a lipid signature deriving primarily from plant waxes and root components (C20C32). Solid-state (13)C NMR spectra of adipocere displayed well-resolved signals of saturated aliphatic chains and a signal that corresponded to carboxylic acid groups. The NMR spectra of the black humic material revealed signals characteristic of long aliphatic chains. The intensities varied in relation to the state of degradation of the sample, as did the signals of oxidized aliphatic chains, acetals and ketals, aromatic structures, esters and amids. The analyses confirmed that the black humic material was indeed derived from adipocere, so the assumption is that the components detected must have developed from aliphatic fatty acids via a number of oxidation and condensation processes. We therefore propose the existence of chemical pathway(s) for the degradation of adipocere under poikiloaerobic conditions. Possible (biogeo)chemical reaction chains include (1) the autoxidation of fatty acids enhanced by haemoglobin, methaemoglobin and haemin, (2) the use of alternative electron acceptors, which leads to the formation of H2S that then reacts abiotically with iron (from haemoglobin), rendering iron sulphide, and (3) the Maillard reaction. These findings are another step forward in understanding the chemistry of buried corpses.

Regulation of insulin secretion, glucokinase gene transcription and beta cell proliferation by adipocyte-derived Wnt signalling molecules.

AIMS/HYPOTHESIS: Adipocytes secrete signalling molecules that elicit responses from target cells, including pancreatic beta cells. Wnt signalling molecules have recently been identified as novel adipocyte-derived factors. They also regulate insulin secretion in pancreatic beta cells and the cell cycle. The aim of this study was to investigate the effect of adipocyte-derived Wnt signalling molecules on insulin secretion and beta cell proliferation. METHODS: Human adipocytes were isolated to generate fat cell-conditioned medium (FCCM). Ins-1 cells were stimulated with FCCM and transiently transfected with reporter genes. Proliferation assays using [3H]thymidine incorporation were carried out in Ins-1 cells and primary islet cells. Insulin secretion from primary islets was assessed by radioimmunoassay. Gene expression in primary islets was assessed by Taqman PCR. RESULTS: Treatment with human FCCM increased the transcription of a T cell-specific transcription factor reporter gene (TOPFLASH) in Ins-1 cells (241%, p < 0.05). FCCM induced the proliferation of Ins-1 cells (1.8 fold, p < 0.05) and primary mouse islet cells (1.6 fold, p < 0.05). Antagonizing Wnt signalling with secreted Frizzled-related protein 1 (FRP-1) inhibited the proliferative effect induced by Wnt3a and FCCM on Ins-1 cells by 49 and 41%, respectively. In addition, FCCM led to a twofold (p < 0.05) induction of cyclin D1 promoter activity in Ins-1 cells. Furthermore, FCCM stimulated insulin secretion (204% of controls, p > 0.05) in primary mouse islets, and this stimulation was inhibited by sFRP-1. At a molecular level, canonical Wnt signalling induced glucokinase gene transcription in a peroxisome proliferator-activated receptor gamma-dependent fashion, thereby defining the glucokinase gene as a novel Wnt target gene. CONCLUSIONS/INTERPRETATION: Taken together, these data show that adipocyte-derived Wnt signalling molecules induce beta cell proliferation and insulin secretion in vitro, suggesting a novel mechanism linking obesity to hyperinsulinaemia.