Vitamin D and pancreatic islet function I. Time course for changes in insulin secretion and content during vitamin D deprivation and repletion

Labriji-Mestaghanmi, H.; Billaudel, B.; Garnier, Philippe; Malaisse, Willy; Sutter, B. C. J.

doi:10.1007/bf03350185

Cited by 38 publications

(28 citation statements)

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“…Rats were housed in a dark room and had free access to food and water. As previously described (Labriji-Mestaghanmi et al 1988, Bourlon et al 1996 such a 4-week vitamin D 3 deficiency induced rachitism, with a smaller body weight ( 0·3), hypoglycaemia ( 0·7), and relative hypocalcaemia ( 0·8). Pancreatic islets were isolated by collagenase digestion (Lacy & Kostianovsky 1967).…”

Section: Animals and Isolation Of Islets Of Langerhansmentioning

confidence: 62%

“…The rat endocrine pancreas is one of these non-classical target tissues presenting 1,25(OH) 2 D 3 receptors ( Johnson et al 1994), even in vitamin D 3 -deficient rats (Clark et al 1980, Ishida & Norman 1988. Several studies have demonstrated a regulatory role for 1,25(OH) 2 D 3 in improving the insulin release that is dramatically reduced by vitamin D 3 deficiency (Norman et al 1980, Clark et al 1981, Chertow et al 1983, Labriji-Mestaghanmi et al 1988. 1,25(OH) 2 D 3 acts, at least in part, as a steroid in numerous tissues.…”

Section: Introductionmentioning

confidence: 99%

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The de novo synthesis of numerous proteins is decreased during vitamin D3 deficiency and is gradually restored by 1, 25-dihydroxyvitamin D3 repletion in the islets of langerhans of rats

Bourlon¹,

Faure-Dussert²,

Billaudel³

1999

Journal of Endocrinology

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Since both the release and de novo biosynthesis of insulin are severely decreased by vitamin D 3 deficiency and improved by 1,25-dihydroxyvitamin D 3 (1,25(OH) 2 D 3 ) repletion following a 6-h delay in the rat, the present experiments investigated the effects of vitamin D 3 deficiency on the biosynthesis of heavier molecular weight proteins using electrophoretic separation. Gel protein staining by Coomassie blue showed very different profiles for islets protein production from 4-week vitamin D 3 -deficient rats compared with normal islets. The pattern was characterised by a decrease in high molecular weight proteins, concomitantly accompanied by an increase in low molecular weight proteins. This tendency was partially reversed in vivo by 1,25(OH) 2 D 3 repletion treatment for 7 days and was evident after only 16 h of treatment.In parallel with these in vivo observations, which represent a static index of islets protein production, a kinetic study was performed in vitro by a double-labelling method allowing us to measure the de novo synthesis of proteins in islets during a strong 16·7 mM glucose stimulation. Comparison of 3 H and 14 C labelled samples was achieved via coelectrophoresis to avoid experimental artefacts. The study of the ratio of d.p.m.3 H/d.p.m. 14 C for each molecular weight protein in islets stimulated by 16·7 mM glucose (versus basal 4·2 mM glucose) showed an increase in the height of certain peaks: 150, 130 and 8·5 kDa.Under the same conditions, islets from 4-week vitamin D 3 -deficient rats (versus normal islets) presented a large deficit of numerous newly synthesised proteins and particularly those implicated in the response to glucose stimulation. In vitro repletion of 1,25(OH) 2 D 3 tended to reverse, at least in part, the deleterious effect of vitamin D 3 deficiency on the de novo protein synthesis of islets but these effects were gradual. Indeed, there was no detectable effect at 2 h incubation, but 1,25(OH) 2 D 3 increased the 60 to 65 kDa, 55 kDa, and 9 to 8 kDa molecular mass proteins at 4 h, and increased the level of most newly synthesised proteins at 6 h. These data support the hypothesis of a beneficial genomic influence of 1,25(OH) 2 D 3 that occurs progressively within the islets of Langerhans and which may prepare the cells for an enhanced response to glucose stimulation.

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Section: Animals and Isolation Of Islets Of Langerhansmentioning

confidence: 62%

Section: Introductionmentioning

confidence: 99%

The de novo synthesis of numerous proteins is decreased during vitamin D3 deficiency and is gradually restored by 1, 25-dihydroxyvitamin D3 repletion in the islets of langerhans of rats

Bourlon¹,

Faure-Dussert²,

Billaudel³

1999

Journal of Endocrinology

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“…Also, Kadowaki and Norman [17] in isolated perfused rat pancreas and Cade and Norman [21] in rats have demonstrated that vitamin D deficiency reduces only the peak of monophasic insulin response induced by boluses o f tolbutamide [17] or glucose [21], It is still unclear whether the effect of vitamin D on insulin secretion is due to a direct action on pancreatic [1-cell or to elevation o f serum calcium levels. Some studies in animals [17][18][19] have excluded hypocalcemia as a possible cause of inhibition of insulin secretion in the vitamin Ddeficient state and Mak [27] and Quesada et al [25] have in M H patients found an increase in glucose-induced insulin secretion after calcitriol administration despite the lack of changes in serum calcium levels. On the contrary, Tanaka et al [34] in in vivo and perfusion experiments have found that calcium, not la,25(HO)2-vitamin D 3, is essential for the reversal o f impaired insulin release in vitamin D-deficient rats.…”

Section: Discussionmentioning

confidence: 99%

Glucose-Induced Insulin Secretion in Uremia: Role of 1α,25(HO)<sub>2</sub>-Vitamin D<sub>3</sub>

Allegra¹,

Luisetto²,

Mengozzi³

et al. 1994

Nephron

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To evaluate the role and mechanism of action of calcitriol on glucose-induced insulin secretion in uremia, 17 patients with severe chronic renal failure were studied. Glucose metabolism was investigated by the intravenous glucose tolerance test (IVGTT) before and after treatment for 21 days with 0.5 µg/day of calcitriol and 500 mg/day of calcium (C + Ca) (6 cases) or 0.5 µg/day of calcitriol alone (C) (11 cases). After these evaluations the patients on C + Ca were shifted to C and 6 patients on C were shifted to C + Ca, and IVGTT was repeated 21 days after the shift. For each test plasma glucose (G), immunoreactive insulin (IRI) and C-peptide (C-p) were measured at -30,0,2,5,15,30,45,60 min, and baseline plasma values of 1α,25(HO)₂-vitamin D₃, C-terminal parathyroid hormone (PTH-C), intact parathyroid hormone (PTH-I), calcitonin, and serum values of total and ionized calcium were dosed. Also, glucose constant decay (K-G), insulin response (IRI area), C-p production (C-p area), insulinogenic index (IGI) and insulin resistance index (RI) were calculated. A historical group of 21 healthy volunteers formed the normal controls. 1α,25(HO)₂-vitamin D₃ plasma levels in uremic patients before treatment were significantly lower than normal range. As compared to controls, uremic patients showed significantly lower K-G, IRI area and IGI values and significantly higher RI values. After treatment with C or C + Ca, the insulin response improved significantly at 2 and 5 min and G decrement was more marked at 30,45 and 60 min. K-G and 0-15 min IRI area, 0-15 min IGI and 0-15 min C-p area values increased significantly but did not reach the normal values. Serum calcium and plasma 1α,25(HO)₂-vitamin D₃ levels significantly increased after treatment but no correlations were found between changes in glucose metabolism parameters and changes in total or ionized serum calcium or changes in 1α,25(HO)₂-vitamin D₃ plasma levels. Serum calcium values significantly decreased after shift from C + Ca to C and significantly increased after shift from C to C + Ca, but glucose metabolism parameters showed no further changes. From these data we inferred that 1α,25(HO)₂-vitamin D₃ deficiency may contribute to the inhibition of glucose-induced insulin secretion in uremia. Calcitriol mainly influences the first phase of insulin release and its effect may be due to a direct action on the pancreatic β-cell.

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“…Vitamin D and metabolic diseases (33)(34)(35)(36)(37) and IR (7,33,34) , the primary underlying defects characterising T2D. It has also been reported that direct action of 1,25-dihydroxyvitamin D, may lead to increased expression of insulin receptor and enhanced insulin responsiveness for GLUT (38,39) .…”

Section: Commentmentioning

confidence: 99%

Vitamin D, type 2 diabetes and other metabolic outcomes: a systematic review and meta-analysis of prospective studies

et al. 2012

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Vitamin D status may influence the risk of developing metabolic diseases such as Type 2 diabetes (T2D), metabolic syndrome (MetS) and insulin resistance (IR). Several studies have assessed vitamin D in relationship with metabolic outcomes; however, results remain inconsistent. A systematic review and meta-analysis using multiple databases (MEDLINE, Web of Science and EMBASE), was performed up to 10 August 2012. Prospective studies reporting association of circulating or dietary vitamin D with incident T2D, MetS and IR outcomes were included. Relative risks (RR) were pooled using random effects and subgroup analysis by pertinent study-level characteristics was performed. A total of seventeen articles based on eighteen unique prospective studies, and comprising 210 107 participants with 15 899 metabolic events, collected during a median follow up of 10 years (range 3-22 years), were included. RR for individuals in top v. bottom thirds of baseline vitamin D were 0 . 81 (95 % CI 0 . 71, 0 . 92); 0 . 86 (95 % CI 0 . 80, 0 . 92); and 0 . 84 (95 % CI 0 . 64, 1 . 12) for T2D, MetS and IR outcomes, respectively. Moderate heterogeneity was found between fourteen studies (I 2 = 67 %, P < 0 . 001) reporting on T2D. Findings were generally consistent across various study-level characteristics. In conclusion, vitamin D status at baseline in apparently healthy adults is inversely associated with future risks of T2D and MetS. Interventions aimed at maintaining adequate levels of vitamin D in addition to preventing deficiency may be a useful preventive measure for metabolic diseases. However, reliable evidence from carefully designed intervention studies, particularly those based on healthy populations, is needed to confirm observational findings.

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Vitamin D and pancreatic islet function I. Time course for changes in insulin secretion and content during vitamin D deprivation and repletion

Cited by 38 publications

References 21 publications

The de novo synthesis of numerous proteins is decreased during vitamin D3 deficiency and is gradually restored by 1, 25-dihydroxyvitamin D3 repletion in the islets of langerhans of rats

The de novo synthesis of numerous proteins is decreased during vitamin D3 deficiency and is gradually restored by 1, 25-dihydroxyvitamin D3 repletion in the islets of langerhans of rats

Glucose-Induced Insulin Secretion in Uremia: Role of 1α,25(HO)<sub>2</sub>-Vitamin D<sub>3</sub>

Vitamin D, type 2 diabetes and other metabolic outcomes: a systematic review and meta-analysis of prospective studies

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