{'fraction_non_alphanumeric': 0.02489229296314026, 'fraction_numerical': 0.01244614648157013, 'mean_word_length': 5.53125, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
The genetics of type 2 diabetes.

Of the various subtypes of diabetes, type 2 diabetes has the greatest impact on health worldwide. Around 150 million people have type 2 diabetes, and the prevalence will rise by 40% by 2010 [1]. Type 2 diabetes and its complications already consume 5±10% of health budgets in many countries [2]. Yet, despite the manifest importance of this condition, and many years of detailed metabolic study, understanding of the basic aetiological mechanisms remains fragmentary [3]. This contrasts with the other major subtype of diabetes, type 1, where it is wellestablished that the major aetiological process involves autoimmune destruction of the insulin-secreting pancreatic beta-cells. Type 2 diabetes displays a clear association with obesity, and the clustering of type 2 diabetes, hypertension, dyslipidaemia and macrovascular disease within individuals and families, indicates that reduced sensitivity to the peripheral actions of insulin (i.e. insulin resistance) plays a key role in disease pathogenesis [4]. However, since many individuals with marked insulin resistance still manage to maintain normal glucose homeostasis, variation in the compensatory capacity of the pancreatic beta-cell must be an equal partner in disease progression [5]. Efforts to characterize further the crucial intermediate metabolic steps in the development of full-blown type 2 diabetes have largely foundered on the rocks of individual heterogeneity and the complicating effects of hyperglycaemia (and its treatment) on the very intermediate traits that investigators might wish to measure. Improved glycaemic control has been clearly shown to reduce the burden of diabetic complications [6]. Since currently available treatments rarely achieve the goal of lifelong restoration of normoglycaemia, there is manifest need for improved therapeutic and preventative modalities targeted to the key pathogenetic steps. As with the other complex inherited traits, the hope is that genetic analyses will deliver the molecular understanding that will inform future drug development.