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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=SLC30A8</id>
	<title>SLC30A8 - История изменений</title>
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	<updated>2026-05-18T16:23:42Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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		<id>https://transhumanist.ru/index.php?title=SLC30A8&amp;diff=5521&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «Zinc transporter 8 (ZnT-8) (Solute carrier family 30 member 8) [ZNT8]  ==Publications==  {{medline-entry |title=The risk allele load accelerates the age-dependent...»</title>
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		<updated>2021-05-12T13:47:59Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «Zinc transporter 8 (ZnT-8) (Solute carrier family 30 member 8) [ZNT8]  ==Publications==  {{medline-entry |title=The risk allele load accelerates the age-dependent...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Zinc transporter 8 (ZnT-8) (Solute carrier family 30 member 8) [ZNT8]&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=The risk allele load accelerates the age-dependent decline in beta cell function.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/19172244&lt;br /&gt;
|abstract=Among the novel type 2 diabetes risk loci identified by genome-wide association studies, [[TCF7L2]], [[HHEX]], [[SLC30A8]] and [[CDKAL1]] appear to affect beta cell function. In the present study we examined the effect of these genes&amp;#039; risk alleles on the age-dependent decline in insulin secretion. The SNPs rs7903146 ([[TCF7L2]]), rs7754840([[CDKAL1]]), rs7923837 ([[HHEX]]) and rs13266634 ([[SLC30A8]]) were genotyped in 1,412 non-diabetic patients, who were subsequently grouped according to their number of risk alleles. All participants underwent an OGTT. Insulin secretion was assessed by validated indices and proinsulin conversion by calculating AUC(proinsulin)/AUC(insulin). The number of risk alleles revealed a Gaussian distribution, with most participants carrying four risk alleles. Stratification into groups with low (LAL, up to three alleles), median ([[MAL]], four alleles) and high ([[HAL]], five to eight alleles) allele load resulted in [[MAL]] and [[HAL]] participants displaying significantly lower insulin secretion and proinsulin conversion than LAL participants (p &amp;lt;or= 0.0014 and p = 0.0185, respectively). In the overall cohort, age was negatively associated with insulin secretion and proinsulin conversion (both p &amp;lt; 0.0001). [[MAL]] and [[HAL]] participants showed a significantly more pronounced decline in insulin secretion with increasing age than LAL participants (p &amp;lt;or= 0.0325; analysis of covariance), and after stratification for BMI this relationship was maintained in obese, but not non-obese, participants. Proinsulin conversion decreased with increasing age in [[MAL]] and [[HAL]], but not LAL, participants (p &amp;lt;or= 0.0003 vs p = 0.2). The risk allele load significantly accelerates the age-dependent decline in beta cell function, and this might be of particular importance in obese people.&lt;br /&gt;
|mesh-terms=* Adult&lt;br /&gt;
* Aging&lt;br /&gt;
* Analysis of Variance&lt;br /&gt;
* Blood Glucose&lt;br /&gt;
* Body Mass Index&lt;br /&gt;
* DNA&lt;br /&gt;
* Diabetes Mellitus, Type 2&lt;br /&gt;
* Female&lt;br /&gt;
* Gene Frequency&lt;br /&gt;
* Genome, Human&lt;br /&gt;
* Genotype&lt;br /&gt;
* Germany&lt;br /&gt;
* Glucose Tolerance Test&lt;br /&gt;
* Humans&lt;br /&gt;
* Insulin-Secreting Cells&lt;br /&gt;
* Male&lt;br /&gt;
* Polymorphism, Single Nucleotide&lt;br /&gt;
* Risk Assessment&lt;br /&gt;
&lt;br /&gt;
|full-text-url=https://sci-hub.do/10.1007/s00125-008-1250-2&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
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