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Studies of the past decade have increased our understanding of the role of adipose tissue dysfunction in obesity and obesity-related insulin resistance and type 2 diabetes. Although adipose tissue is the body's largest pool of free cholesterol, adipocytes have limited activity in cholesterol synthetic pathway. Thus, the majority of adipocyte cholesterol originates from circulating lipoproteins. To maintain cholesterol homeostasis, adipocytes have developed multiple pathways for cholesterol efflux. Several transcriptional factors, such as sterol regulatory element-binding proteins and liver X receptors may be responsible for the regulation of cholesterol homeostasis in adipocytes. Most notably, because altering cholesterol balance profoundly modifies adipocyte metabolism in a way resembling that seen in hypertrophied adipocytes, cholesterol imbalance is recognized as a characteristic for enlarged adipocytes per se in the obese state. In addition, plasma membrane cholesterol normalization by chromium picolinate can fully restore insulin-stimulated glucose transport, further supporting the role of the adipocyte cholesterol imbalance in obesity and insulin resistance.

Olfactory neuroblastoma (ON, esthesioneuroblastoma) is a high-grade malignant tumour of neuronal origin. Little is known about the neurobiological behaviour of this tumour. Ten cases of ON and five cases of nasopharyngeal carcinoma were examined for expression of trkA and p75 neurotrophin receptor (p75NTR) using immunohistochemistry and double labelling fluorescence. We found that all ON tissues from 10 cases expressed both trkA and p75NTR at different levels. Double staining revealed that almost all trkA-immunoreactive ON cells also contained p75NTR immunoreactivity. By contrast, no trkA or p75NTR immunoreactivity was detected in nasopharyngeal carcinoma cells from five patients. These results suggest that nerve growth factor may play a role in the generation of ON and staining of trkA and p75NTR may assist in the diagnosis of ON.