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To implement a custom type, implement either org.hibernate.UserType or org.hibernate.CompositeUserType and declare properties using the fully qualified classname of the type. View org.hibernate.test.DoubleStringType to see the kind of things that are possible.

Notice the use of <column> tags to map a property to multiple columns.

The CompositeUserType , EnhancedUserType , UserCollectionType , and UserVersionType interfaces provide support for more specialized uses.

You can even supply parameters to a UserType in the mapping file. To do this, your UserType must implement the org.hibernate.usertype.ParameterizedType interface. To supply parameters to your custom type, you can use the <type> element in your mapping files.

The UserType can now retrieve the value for the parameter named default from the Properties object passed to it.

If you regularly use a certain UserType , it is useful to define a shorter name for it. You can do this using the <typedef> element. Typedefs assign a name to a custom type, and can also contain a list of default parameter values if the type is parameterized.

It is also possible to override the parameters supplied in a typedef on a case-by-case basis by using type parameters on the property mapping.

Even though Hibernate's rich range of built-in types and support for components means you will rarely need to use a custom type, it is considered good practice to use custom types for non-entity classes that occur frequently in your application. For example, a MonetaryAmount class is a good candidate for a CompositeUserType , even though it could be mapped as a component. One reason for this is abstraction. With a custom type, your mapping documents would be protected against changes to the way monetary values are represented.

It is possible to provide more than one mapping for a particular persistent class. In this case, you must specify an entity name to disambiguate between instances of the two mapped entities. By default, the entity name is the same as the class name. Hibernate lets you specify the entity name when working with persistent objects, when writing queries, or when mapping associations to the named entity.

Associations are now specified using entity-name instead of class .

You can force Hibernate to quote an identifier in the generated SQL by enclosing the table or column name in backticks in the mapping document. Hibernate will use the correct quotation style for the SQL Dialect . This is usually double quotes, but the SQL Server uses brackets and MySQL uses backticks.

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Section 3: Phasic Insulin Release and Metabolic Control

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Diabetes 2002 Feb; 51 (suppl 1): S117 - S121. https://doi.org/10.2337/diabetes.51.2007.S117
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Abstract

Insulin is released from the pancreas in a biphasic manner in response to a square-wave increase in arterial glucose concentration. The first phase consists of a brief spike lasting ∼10 min followed by the second phase, which reaches a plateau at 2–3 h. It is widely thought that diminution of first-phase insulin release is the earliest detectable defect of β-cell function in individuals destined to develop type 2 diabetes and that this defect largely represents β-cell exhaustion after years of compensation for antecedent insulin resistance. In this article, the origins of these concepts are reviewed and recent evidence is presented suggesting that reductions in both phases of insulin release are equally early, that they precede insulin resistance other than that simply due to obesity, and that they therefore may represent the primary genetic risk factor predisposing individuals to type 2 diabetes.

The kinetics of insulin release and its implications for normal physiology and the pathogenesis of type 2 diabetes were the main themes of this symposium. It has been known for nearly 40 years that insulin secretion is biphasic ( 1 ) (i.e., in response to a square-wave hyperglycemic stimulus to either the in vitro perfused rat pancreas or the in vivo human pancreas) and that insulin concentrations in perfusate and plasma increase rapidly to a peak at 2–4 min, decrease to a nadir at 10–15 min, and then gradually increase progressively to a pseudo-steady state at 2–3 h. The initial spike response is generally referred to as first-phase insulin release, and the subsequent increase in insulin secretion is considered to represent the second-phase insulin release.

The earliest detectable defect in β-cell function is commonly thought to be a reduction in first-phase insulin release ( 2 ). This concept arose largely based on cross-sectional studies of individuals with various degrees of glucose tolerance that examined only first-phase insulin responses after intravenous injection of insulin. These studies found that first-phase insulin was reduced in individuals with plasma glucose in upper ranges of normal and was essentially absent in people with fasting hyperglycemia ( 3 , 4 ). The concept received further support from studies of people with impaired glucose tolerance (IGT), a precursor of type 2 diabetes, showing that these individuals generally had reduced plasma insulin levels at 30 min after glucose ingestion and “normal or increased” plasma insulin levels at 120 min ( 5 ). The assumption has been generally made that the 30-min response reflected first-phase insulin release, whereas the 120-min response reflected second-phase insulin release. Because insulin released early after glucose ingestion has been shown to be a key determinant of subsequent plasma glucose responses ( 6 , 7 ), it became widely accepted that reduced first-phase insulin release is responsible for the development of IGT.

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