The basal oxygen consumption in thyrotoxicosis, as measured by the BMR, is elevated. The increase is above the level of metabolism that the person would have if he or she were not thyrotoxic. In extreme thyrotoxicosis, the BMR may be double the standard, that is, according to the usual mode of expression, + 100. In moderately severe thyrotoxicosis it may be from +30 to +60, and in mild thyrotoxicosis from +10 to +30.
In addition to the BMR, one should consider the total metabolism, that is the basal plus the increments occasioned by work, food, or emotion. An increased cost of muscular work in thyrotoxicosis was reported many years ago by Plummer and Boothby [409] and Briard et al. [410] among others. These studies, whose results have been disputed, suggested that the thyrotoxic subject has less efficient coupling of oxidation and energy use than either the normal subject or, for example, the hypermetabolic patient with leukemia. Some recent studies indicate that the increase in energy expenditure caused by work is not altered by thyrotoxicosis [411], and other studies support the original observations.
CARBOHYDRATE METABOLISM
Absorption of carbohydrate from the intestine is accelerated, as is its removal from the plasma. After a standard oral glucose load is given, the thyrotoxic patient characteristically has an early and rapid rise in blood glucose concentration in 30 - 60 minutes (possibly to more than 200 mg/dl) and a rapid fall, so that by two hours the concentration is normal. The early peak may be associated with glycosuria. Intravenous administration does not usually elevate the blood glucose level beyond the rise found in normal subjects.
Thyrotoxicosis increases the demand for insulin, perhaps by accelerating its metabolism. In addition, resistance to the action of insulin is present, since in nondiabetic thyrotoxic patients normal fasting blood glucose levels are associated with double the normal insulin concentration [412], and resistance is found on incubation of adipocytes in vitro [413]. Diabetes may be activated or intensified, and is ameliorated or may disappear when the thyrotoxicosis is treated. Long ago experimental diabetes was shown to result from long-standing thyrotoxicosis in the presence of partial pancreatectomy [414]. The adverse effect of hyperthyroidism on glucose control in patients with non-insulin dependent diabetes is caused by increased basal hepatic glucose production and reduced ability of insulin and glucose to suppress hepatic glucose production [415, 416]. Although hyperthyroidism increases the requirement for insulin, the effectiveness of exogenous insulin on carbohydrate metabolism is actually enhanced. If glucose is administered intravenously and continuously to a thyrotoxic subject so that blood sugar is maintained at a high level, administered insulin has an effect on glucose removal from the blood [416] that is greater than that in the normal subject.
Type I diabetes mellitus co-occurs with increased frequency in autoimmune thyroid disease. Post-partum thyroid dysfunction is especially common in patients with diabetes [417]. In recent years many similarities in immunologic phenomena have been noted in the two diseases, including insulin receptor antibodies and islet cell antibodies.
Effect of thyroid hormones on blood glucose
connection between iron metabolism and hypothiroidsim
Peripheral Thyroid Hormone Conversion and Its Impact on TSH and Metabolic Activity: 
