Effect of hypocalcaemia on glucose tolerance, insulin release and free fatty acid levels in human subjects

Abstract

SummaryEight patients with hypocalcaemia who presented with frank or latent tetany due to parathyroid insufficiency or nutritional osteomalacia were studied. Their serum calcium ranged from 6'85 to 7 7 mg/100 ml (mean 7-33±0-36 mg/100 ml). In six of them, serum calcium after treatment varied from 8 4 to 9-2 mg/100 ml. In ten healthy normal subjects the serum calcium levels were 9 0-10'2 mg/100 ml (9'50±0 47 mg/100 ml). The blood glucose levels during a 3 hr oral GTT were significantly elevated during hypocalcaemia and returned to normal levels after treatment. Serum insulin levels were low at 60 and 120 min after the administration of glucose in hypocalcaemia but returned to normal once the serum calcium levels were above 8-4 mg/100 ml. The FFA levels were high during the low calcium state and reached normal levels after treatment. The above studies suggest that an optimal level of serum calcium is essential for glucose-induced insulin release.

Glucose intolerance and impairment of insulin secretion in relation to vitamin D deficiency in East London Asians

“…It has been suggested that disorders which increase in prevalence with increasing latitude, and present more commonly in winter, such as ischaemic heart disease, could prove to relate to vitamin D deficiency [30]. This suggestion is supported by the reductions in NEFA concentrations [9,21] and in insulin resistance [9] reported with correction of vitamin D depletion in man, to which secondary hyperparathyroidism has been suggested to contribute [31]. Examination of dietary information from the survey of which the present study is a part has shown initial serum 25-hydroxy-vitamin D concentrations in at-risk subjects at OGTT to be related to the consumption of fish; a relationship found in both at-risk and not-at-risk subjects (p < 0.04 and < 0.02, respectively) [14].…”

“…It is possible, therefore, that longterm vitamin D depletion could contribute to the increased prevalence of diabetes seen in Asians migrating to Northern Europe as compared to that of indigenous Caucasians. Early correction of vitamin D depletion has been shown to restore both insulin secretion and normoglycaemia in dialysis patients developing glucose intolerance with failing 1-hydroxylation of 25-hydroxy-vitamin D [6,23] and in earlier case reports of treatment of vitamin D deficiency in subjects with glucose intolerance [9]. As in previous reports of treatment with vitamin D or its active di-hydroxy form in four vitamin D-depleted patients with established diabetes [17], and in 35 patients with NIDDM [24], we found no improvement in abnormal glucose tolerance in our 22 vitamin D-treated subjects despite improvement in insulin output.…”

“…While not all the at-risk subjects identified in the present survey agreed to OGTT, and not all attenders for OGTT agreed to full venous sampling, a problem also found in communities in India [15], the numbers studied were sufficient to demonstrate a relationship between vitamin D status and both insulin and C-peptide concentrations at 30 min on OGTT, reflecting secretion/release into the bloodstream, in subjects at-risk and not-at-risk of diabetes at screening. Vitamin D has been shown to be required for maintenance of normal glucose tolerance and insulin release in animals [4,5], and is believed to act in the same way in man, possibly by ensuring the availability of free calcium ions [9,16]. Prolonged depletion leads to failure of insulin secretion which over time becomes irreversible [17].…”

“…Administration of 1,25 calcitriol improves insulin secretion and corrects early glucose intolerance in patients with renal failure [6]. Calcium appears to be necessary for normal insulin secretion [7,8] and correction of hypocalcaemia in nutritional rickets and hypoparathyroidism has been shown to correct both insulin secretion and impaired glucose tolerance in a group of eight patients [9]. We therefore examined the vitamin D status by oral glucose tolerance test (OGTT) of subjects screened as "atrisk" of diabetes, during a study of dietary factors in diabetes aetiology in East London Asians.…”

Effect of acute hypercalcaemia on glucose tolerance and insulin release in human beings

“…The presence of a sufficient amount of extracellular calcium is required for glucose to stimulate insulin secretion in the pancreatic beta cell (Grodsky & Bennett 1966;Milner & Hales 1967;Curry et al 1968;Malaisse et al 1970;Charles et al 1975;Malaisse 1972;Hellmann 1975;Witzel & Littledike 1973;Littledike et al 1968). It has been demonstrated by Gedik & Zileli (1977) and other investigators (Bansal et al 1975;Laron & Rosenberg 1970;Yasuda et al 1975) that in the hypocalcaemic state, insulin secretion and glucose tolerance are reversibly impaired in human beings.…”