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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

 (a,b) Comparisons of the relative volumes of α‐and β‐cells and the A/B ratio (α‐cell area/β‐cell area) in islets among groups, respectively. (a) The β‐cell fraction in the islet area in diabetic patients was significantly decreased compared with other groups (*P < 0.05). but the α‐cell fraction was increased in diabetic patients (†P < 0.05) (adapted from Yoon et al.). Non‐α and non‐β endocrine cell area in islets did not differ between groups. (b) A/B ratio was increased in diabetic patients compared with other groups (‡P < 0.05) (adapted from Yoon et al., Copyright 2003, The Endocrine Society).
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f5:  (a,b) Comparisons of the relative volumes of α‐and β‐cells and the A/B ratio (α‐cell area/β‐cell area) in islets among groups, respectively. (a) The β‐cell fraction in the islet area in diabetic patients was significantly decreased compared with other groups (*P < 0.05). but the α‐cell fraction was increased in diabetic patients (†P < 0.05) (adapted from Yoon et al.). Non‐α and non‐β endocrine cell area in islets did not differ between groups. (b) A/B ratio was increased in diabetic patients compared with other groups (‡P < 0.05) (adapted from Yoon et al., Copyright 2003, The Endocrine Society).

Mentions: Interestingly, in contrast to the changes in β‐cell mass, dysregulation of glucagon secretion or the disproportionately increased number of α‐cells relative to β‐cells in these individuals can contribute to hyperglycemia11,17–22. Müller et al.17 showed an unsuppressed glucagon response to a carbohydrate meal in type 2 diabetes. Unger et al. identified relative or absolute hyperglucagonemia in every form of endogeneous hyperglycemia and reported that such a glucagon excess could be a principal factor in the overproduction of glucose in diabetes8. We reported that the α‐cell mass was clearly increased in type 2 diabetic patients relative to the normal subjects. The ratio of α‐cell area to β‐cell area was far more profoundly increased in type 2 diabetic patients (Figure 5)11. As a mechanism of increase in α‐cell mass, O’Reilly et al.23 previously observed α‐cell neogenesis in an animal model. Ellingsgaard et al. reported that α‐cell expansion was regulated by IL‐6 in human islets, which is systemically elevated in obesity and is a predictive factor to developing type 2 diabetes. IL‐6 was associated with α‐cell proliferation and the prevention of α‐cell apoptosis24. We suggest α‐cell neogenesis or replication also could be developed together with β‐cell neogenesis or replication (Figure 2). However, it is not fully understood why α‐cell mass is increased. It is also not known why increased α‐cell mass is closely associated with hyperglucagonemia or unsuppressed glucagon response. So further studies on α‐cell mass and dysfunction are needed.


β-cell mass in people with type 2 diabetes.

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

 (a,b) Comparisons of the relative volumes of α‐and β‐cells and the A/B ratio (α‐cell area/β‐cell area) in islets among groups, respectively. (a) The β‐cell fraction in the islet area in diabetic patients was significantly decreased compared with other groups (*P < 0.05). but the α‐cell fraction was increased in diabetic patients (†P < 0.05) (adapted from Yoon et al.). Non‐α and non‐β endocrine cell area in islets did not differ between groups. (b) A/B ratio was increased in diabetic patients compared with other groups (‡P < 0.05) (adapted from Yoon et al., Copyright 2003, The Endocrine Society).
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4008010&req=5

f5:  (a,b) Comparisons of the relative volumes of α‐and β‐cells and the A/B ratio (α‐cell area/β‐cell area) in islets among groups, respectively. (a) The β‐cell fraction in the islet area in diabetic patients was significantly decreased compared with other groups (*P < 0.05). but the α‐cell fraction was increased in diabetic patients (†P < 0.05) (adapted from Yoon et al.). Non‐α and non‐β endocrine cell area in islets did not differ between groups. (b) A/B ratio was increased in diabetic patients compared with other groups (‡P < 0.05) (adapted from Yoon et al., Copyright 2003, The Endocrine Society).
Mentions: Interestingly, in contrast to the changes in β‐cell mass, dysregulation of glucagon secretion or the disproportionately increased number of α‐cells relative to β‐cells in these individuals can contribute to hyperglycemia11,17–22. Müller et al.17 showed an unsuppressed glucagon response to a carbohydrate meal in type 2 diabetes. Unger et al. identified relative or absolute hyperglucagonemia in every form of endogeneous hyperglycemia and reported that such a glucagon excess could be a principal factor in the overproduction of glucose in diabetes8. We reported that the α‐cell mass was clearly increased in type 2 diabetic patients relative to the normal subjects. The ratio of α‐cell area to β‐cell area was far more profoundly increased in type 2 diabetic patients (Figure 5)11. As a mechanism of increase in α‐cell mass, O’Reilly et al.23 previously observed α‐cell neogenesis in an animal model. Ellingsgaard et al. reported that α‐cell expansion was regulated by IL‐6 in human islets, which is systemically elevated in obesity and is a predictive factor to developing type 2 diabetes. IL‐6 was associated with α‐cell proliferation and the prevention of α‐cell apoptosis24. We suggest α‐cell neogenesis or replication also could be developed together with β‐cell neogenesis or replication (Figure 2). However, it is not fully understood why α‐cell mass is increased. It is also not known why increased α‐cell mass is closely associated with hyperglucagonemia or unsuppressed glucagon response. So further studies on α‐cell mass and dysfunction are needed.

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