= Solution
\b[<Diabetes> is a disorder of <glucose> regulation with persistent <hyperglycaemia>; the <glycosuria> is a consequence, not a sufficient explanation of its cause.] In 1865 the relation between hepatic <glycogen>, circulating <glucose> and urinary sugar was actively disputed. A contemporary account could reasonably discuss failure to assimilate food and excessive delivery of sugar from the <liver>; it could not possess the later demonstration of <insulin> deficiency. An 1863 discussion of <diabetes> documents competing interpretations of the hepatic experiments, rather than an agreed single lesion.<Book Reviews in the Edinburgh Medical Journal (1863)>[pp. 644–648, review of the 1862 Researches on the Nature and Treatment of Diabetes: competing explanations of hepatic sugar formation]{ref}
In the modern account, <type 1 diabetes> results from destruction of pancreatic <beta cells> and severe deficiency of <insulin>. <Type 2 diabetes> combines <insulin resistance> with inadequate compensatory <insulin secretion>. Disease of the <pancreas> can also cause <diabetes>. Reduced restraint of hepatic <glucose production> and impaired peripheral disposal of <glucose> contribute to <hyperglycaemia>. These mechanisms distinguish types that were not separated in the question's terminology.<What Is Diabetes by NIDDK>[Type 1, type 2 and other types of diabetes]{ref}
When the filtered <glucose> load exceeds renal reabsorptive capacity, <glycosuria> causes an <osmotic diuresis>: loss of water and <electrolytes> produces <polyuria>, <dehydration> and <polydipsia>. Inadequate use of fuels and increased breakdown of stored <fat> and <protein> explain wasting despite appetite. Severe <insulin> deficiency promotes <ketogenesis> and can cause <diabetic ketoacidosis>; it is not correct to make this the inevitable state of everyone with <diabetes>. Conversely, <renal glycosuria> can occur without the systemic metabolic disorder, so a urinary sugar test alone does not settle the diagnosis.<Type 1 Diabetes Mellitus by Merck Manual Professional Edition>[Symptoms and signs; complications: glycosuria and osmotic diuresis]<Acute Complications of Diabetes Mellitus by Merck Manual Professional Edition>[Diabetic ketoacidosis: insulin deficiency and ketogenesis]{ref}
The associated diseases should be separated into predispositions, complications and coincident illnesses. Pulmonary wasting called “phthisis” was prominent in period accounts, but the historical label does not establish that every reported lung cavity was tuberculous.<Book Reviews in the Edinburgh Medical Journal (1863)>[pp. 648–649: discussion of pulmonary disease in diabetes]{ref} Modern <diabetes> increases susceptibility to active <tuberculosis>; it does not convert sugar into tubercle. <Diabetes> also increases susceptibility to some other infections and can accompany recurrent skin infection, poor wound healing and <gangrene>.<TB Risk and People with Diabetes by CDC>[Overview: progression from tuberculosis infection to active disease]{ref} Long-standing <hyperglycaemia> is associated with <retinopathy>, <nephropathy> and <peripheral neuropathy>; accelerated <atherosclerosis> contributes to <coronary artery disease>, <stroke> and limb <ischemia>. <Obesity> is commonly associated with <type 2 diabetes>, although severe untreated disease may cause loss of body mass. None of these associations licenses a claim that every diabetic patient has the same anatomical lesions.<What Is Diabetes by NIDDK>[Health problems associated with diabetes: eye, kidney, nerve and cardiovascular disease]{ref}
For an 1865 investigation, repeated urine testing could demonstrate reducing sugar and its variation with diet; simultaneous study of the <blood> and <liver> was needed to investigate the source. The distinction between <glucose> already present during life and <glucose> formed in an unfixed <liver> after death is crucial experimental design: post-mortem chemical change must not be mistaken for the living organ's output. Modern diagnosis measures <blood glucose> and longer-term glycaemic exposure rather than inferring the entire disorder from the taste or appearance of <urine>.<Type 1 Diabetes Mellitus by Merck Manual Professional Edition>[Diagnosis: plasma glucose, glycated haemoglobin and oral glucose tolerance testing]{ref}
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