Limits...
β-cell mass in people with type 2 diabetes.

Cho JH, Kim JW, Shin JA, Shin J, Yoon KH - J Diabetes Investig (2011)

Bottom Line: Furthermore, β-cell volumes are reduced even in patients with impaired fasting glucose.Such defects in β-cell mass are associated with increased apoptosis rather than insufficient replication or neogenesis of β-cells.With these results, although they still require clarification, the peak β-cell mass might be determined at quite an early stage of life, and then might decline progressively over time as the result of exposure to harmful environmental influences over one's lifetime.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology, Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul, Korea.

ABSTRACT
The early occurrence of β-cell dysfunction has been broadly recognized as a critical determinant of the development and progression of type 2 diabetes. β-cell dysfunction might be induced by insufficient β-cell mass, by a dysfunction of the β-cells, or both. Whether or not β-cell dysfunction constitutes a cause of reduced β-cells or vice-versa currently remains unclear. The results of some studies have measured the loss of β-cells in type 2 diabetic patients at between 22 and 63% by planimetric measurements. Because β-cell hypertrophy has been noted in type 2 diabetic patients, the loss of β-cell number should prove more profound than what has thus far been reported. Furthermore, β-cell volumes are reduced even in patients with impaired fasting glucose. Such defects in β-cell mass are associated with increased apoptosis rather than insufficient replication or neogenesis of β-cells. With these results, although they still require clarification, the peak β-cell mass might be determined at quite an early stage of life, and then might decline progressively over time as the result of exposure to harmful environmental influences over one's lifetime. In this review, we have summarized the relevant studies regarding β-cell mass in patients with type 2 diabetes, and then presented a review of the various causes of β-cell loss in adults. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2010.00072.x, 2010).

No MeSH data available.


Related in: MedlinePlus

 Islet classification according to islet size and β‐cell fraction in the islet: type 1, single β‐cell units or scattered β‐cells; type 2a, small healthy islets; type 2b, small β‐cell‐depleted islets; type 3a, large healthy islets; type 3b, large β‐cell‐depleted islets.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4008010&req=5

f3:  Islet classification according to islet size and β‐cell fraction in the islet: type 1, single β‐cell units or scattered β‐cells; type 2a, small healthy islets; type 2b, small β‐cell‐depleted islets; type 3a, large healthy islets; type 3b, large β‐cell‐depleted islets.

Mentions: Systemic morphological classification of islets is needed to understand the fate of islet over one’s lifetime. We could classify the observed islets into five different types (types 1, 2a, 2b, 3a and 3b) according to islet size and the β‐cell fraction in the islet (Figure 3). Type 1 consisted of single β‐cell units, defined as islets composed of less than three cells, and were recognized as neogenetic loci described earlier15,16. Type 2 consisted of small islets (smaller than 6415 μm2, which is the median size of islets in normal subjects11). Type 3 consisted of large islets (larger than 6415 μm2). An ‘a’ signified islets with normal β‐cell fractions in the islets (more than 0.64, which was the value for the 75th percentile of the total islets in the control group) and a ‘b’ signified β‐cell‐depleted islets (<0.64). The five types of islets are shown in Figure 3. We also measured the islet size and β‐cell areas of all the islets existing in the slide section randomly selected in five subjects with type 2 diabetes (DM group) and nine normal subjects (control group). From these results, we calculated the contribution rate of the β‐cell area within each islet type to the total β‐cell area. The results are shown in Figure 4. The contribution of the type 1 β‐cell area to the total β‐cell area tended to be higher in the DM group than in the control group (10.2 ± 6.0%vs 7.19 ± 4.98%, respectively), whereas the contribution of type 2a was lower in the DM group than in the control group (36.0 ± 3.51%vs 40.0 ± 11.8%, respectively). The contribution of type 3a was significantly lower in the DM group than in the control group (13.4 ± 6.7%vs 31.3 ± 14.6%, respectively; P = 0.025), whereas the contribution of type 3b was significantly higher in the DM group than in the control group (33.9 ± 4.87%vs 17.3 ± 13.2%, respectively; P = 0.020).


β-cell mass in people with type 2 diabetes.

Cho JH, Kim JW, Shin JA, Shin J, Yoon KH - J Diabetes Investig (2011)

 Islet classification according to islet size and β‐cell fraction in the islet: type 1, single β‐cell units or scattered β‐cells; type 2a, small healthy islets; type 2b, small β‐cell‐depleted islets; type 3a, large healthy islets; type 3b, large β‐cell‐depleted islets.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4008010&req=5

f3:  Islet classification according to islet size and β‐cell fraction in the islet: type 1, single β‐cell units or scattered β‐cells; type 2a, small healthy islets; type 2b, small β‐cell‐depleted islets; type 3a, large healthy islets; type 3b, large β‐cell‐depleted islets.
Mentions: Systemic morphological classification of islets is needed to understand the fate of islet over one’s lifetime. We could classify the observed islets into five different types (types 1, 2a, 2b, 3a and 3b) according to islet size and the β‐cell fraction in the islet (Figure 3). Type 1 consisted of single β‐cell units, defined as islets composed of less than three cells, and were recognized as neogenetic loci described earlier15,16. Type 2 consisted of small islets (smaller than 6415 μm2, which is the median size of islets in normal subjects11). Type 3 consisted of large islets (larger than 6415 μm2). An ‘a’ signified islets with normal β‐cell fractions in the islets (more than 0.64, which was the value for the 75th percentile of the total islets in the control group) and a ‘b’ signified β‐cell‐depleted islets (<0.64). The five types of islets are shown in Figure 3. We also measured the islet size and β‐cell areas of all the islets existing in the slide section randomly selected in five subjects with type 2 diabetes (DM group) and nine normal subjects (control group). From these results, we calculated the contribution rate of the β‐cell area within each islet type to the total β‐cell area. The results are shown in Figure 4. The contribution of the type 1 β‐cell area to the total β‐cell area tended to be higher in the DM group than in the control group (10.2 ± 6.0%vs 7.19 ± 4.98%, respectively), whereas the contribution of type 2a was lower in the DM group than in the control group (36.0 ± 3.51%vs 40.0 ± 11.8%, respectively). The contribution of type 3a was significantly lower in the DM group than in the control group (13.4 ± 6.7%vs 31.3 ± 14.6%, respectively; P = 0.025), whereas the contribution of type 3b was significantly higher in the DM group than in the control group (33.9 ± 4.87%vs 17.3 ± 13.2%, respectively; P = 0.020).

Bottom Line: Furthermore, β-cell volumes are reduced even in patients with impaired fasting glucose.Such defects in β-cell mass are associated with increased apoptosis rather than insufficient replication or neogenesis of β-cells.With these results, although they still require clarification, the peak β-cell mass might be determined at quite an early stage of life, and then might decline progressively over time as the result of exposure to harmful environmental influences over one's lifetime.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology, Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul, Korea.

ABSTRACT
The early occurrence of β-cell dysfunction has been broadly recognized as a critical determinant of the development and progression of type 2 diabetes. β-cell dysfunction might be induced by insufficient β-cell mass, by a dysfunction of the β-cells, or both. Whether or not β-cell dysfunction constitutes a cause of reduced β-cells or vice-versa currently remains unclear. The results of some studies have measured the loss of β-cells in type 2 diabetic patients at between 22 and 63% by planimetric measurements. Because β-cell hypertrophy has been noted in type 2 diabetic patients, the loss of β-cell number should prove more profound than what has thus far been reported. Furthermore, β-cell volumes are reduced even in patients with impaired fasting glucose. Such defects in β-cell mass are associated with increased apoptosis rather than insufficient replication or neogenesis of β-cells. With these results, although they still require clarification, the peak β-cell mass might be determined at quite an early stage of life, and then might decline progressively over time as the result of exposure to harmful environmental influences over one's lifetime. In this review, we have summarized the relevant studies regarding β-cell mass in patients with type 2 diabetes, and then presented a review of the various causes of β-cell loss in adults. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2010.00072.x, 2010).

No MeSH data available.


Related in: MedlinePlus