Diabetes is one of the most common chronic diseases at present, and insulin pen injection therapy plays an important role in the treatment of diabetes. However, the majority of patients might reuse disposable insulin pen needles for various reasons, which leads to related complications. As far as we know, this article is the first to describe a patient whose needle remained in the right upper limb while reusing a disposable insulin injection needle for subcutaneous insulin injection with the non-dominant hand. The patient went to the doctor 1 week later. The needle moved from the lateral area of the proximal upper arm (the injection site) to the posterolateral area of the distal upper arm. The needle was then successfully removed by surgery. The reuse of disposable insulin pen needles might lead to serious complications. It is suggested to strengthen the education of people living with diabetes to help them use insulin pen needles safely.
{"title":"Effect of a reused insulin needle remaining in a patient's body","authors":"Yong-jie Qiao, Yu Xin-yuan, Rui-ling Xu, Xiao-yang Song, Shuo Ye, Ping Zhen, Sheng-hu Zhou, Hao-qiang Zhang","doi":"10.1111/jdi.14003","DOIUrl":"https://doi.org/10.1111/jdi.14003","url":null,"abstract":"<p>Diabetes is one of the most common chronic diseases at present, and insulin pen injection therapy plays an important role in the treatment of diabetes. However, the majority of patients might reuse disposable insulin pen needles for various reasons, which leads to related complications. As far as we know, this article is the first to describe a patient whose needle remained in the right upper limb while reusing a disposable insulin injection needle for subcutaneous insulin injection with the non-dominant hand. The patient went to the doctor 1 week later. The needle moved from the lateral area of the proximal upper arm (the injection site) to the posterolateral area of the distal upper arm. The needle was then successfully removed by surgery. The reuse of disposable insulin pen needles might lead to serious complications. It is suggested to strengthen the education of people living with diabetes to help them use insulin pen needles safely.</p>","PeriodicalId":190,"journal":{"name":"Journal of Diabetes Investigation","volume":"14 6","pages":"821-823"},"PeriodicalIF":3.2,"publicationDate":"2023-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.14003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6091535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The decline in β-cell mass due to the failure of β-cell compensation is one cause of the development of type 2 diabetes. Therefore, elucidation of the mechanism by which an adaptive increase in β-cell mass occurs in vivo will lead to the development of a cure for diabetes. Insulin and insulin receptor (IR)-mediated signaling pathways play an important role in the mechanism that increases β-cell mass by compensatory β-cell proliferation in response to chronic insulin resistance. However, whether IR is required for compensatory β-cell proliferation remains controversial in some situations. It might be possible that IR acts as a scaffold for the signaling complex independent of its ligand. It has also been reported that the forkhead box protein M1/polo-like kinase 1/centromere protein A pathway plays a central role in adaptive β-cell proliferation during diet-induced obesity, hyperglycemia, pregnancy, aging and acute insulin resistance. We recently reported that the cross-talk of islets with fat tissue, in addition to the liver, through humoral factors is involved in adaptive β-cell proliferation. This accommodative response of β-cell proliferation through adipocytes was observed particularly under an acute insulin resistance state in an IR/insulin signal-independent and forkhead box protein M1/polo-like kinase 1/centromere protein A pathway-dependent manner. A remaining barrier for the treatment of human diabetes using β-cells is the differences between human and rodent islets. In this review, the focus is on signaling pathways that regulate adaptive β-cell proliferation for the treatment of diabetes considering the abovementioned issues.
{"title":"Signaling pathways that regulate adaptive β-cell proliferation for the treatment of diabetes","authors":"Jun Shirakawa","doi":"10.1111/jdi.14002","DOIUrl":"https://doi.org/10.1111/jdi.14002","url":null,"abstract":"<p>The decline in β-cell mass due to the failure of β-cell compensation is one cause of the development of type 2 diabetes. Therefore, elucidation of the mechanism by which an adaptive increase in β-cell mass occurs <i>in vivo</i> will lead to the development of a cure for diabetes. Insulin and insulin receptor (IR)-mediated signaling pathways play an important role in the mechanism that increases β-cell mass by compensatory β-cell proliferation in response to chronic insulin resistance. However, whether IR is required for compensatory β-cell proliferation remains controversial in some situations. It might be possible that IR acts as a scaffold for the signaling complex independent of its ligand. It has also been reported that the forkhead box protein M1/polo-like kinase 1/centromere protein A pathway plays a central role in adaptive β-cell proliferation during diet-induced obesity, hyperglycemia, pregnancy, aging and acute insulin resistance. We recently reported that the cross-talk of islets with fat tissue, in addition to the liver, through humoral factors is involved in adaptive β-cell proliferation. This accommodative response of β-cell proliferation through adipocytes was observed particularly under an acute insulin resistance state in an IR/insulin signal-independent and forkhead box protein M1/polo-like kinase 1/centromere protein A pathway-dependent manner. A remaining barrier for the treatment of human diabetes using β-cells is the differences between human and rodent islets. In this review, the focus is on signaling pathways that regulate adaptive β-cell proliferation for the treatment of diabetes considering the abovementioned issues.</p>","PeriodicalId":190,"journal":{"name":"Journal of Diabetes Investigation","volume":"14 6","pages":"735-740"},"PeriodicalIF":3.2,"publicationDate":"2023-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.14002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6105183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pancreatic islet transplantation is a β-cell replacement therapy for people with insulin-deficient diabetes who have difficulty in glycemic control and suffer from frequent severe hypoglycemia. However, the number of islet transplantations carried out is still limited in Asia. We report a case of allogeneic islet transplantation in a 45-year-old Japanese man with type 1 diabetes. Although the islet transplantation was successfully carried out, graft loss was observed on the 18th day. Immunosuppressants were used in accordance with the protocol, and donor-specific anti-human leukocyte antigen antibodies were not detected. Autoimmunity relapse was also not observed. However, the patient had a high titer of anti-glutamic acid decarboxylase antibody from before the islet transplantation, and autoimmunity might thus have affected the β-cells in the transplanted islet. The evidence is still scarce to reach conclusions, and further data accumulation is required to enable proper patient selection before islet transplantation.
{"title":"Graft failure after allogeneic islet transplantation in a patient with type 1 diabetes and a high anti-glutamic acid decarboxylase antibody titer","authors":"Noriko Kodani, Daisuke Chujo, Aiko Terakawa, Kyoji Ito, Fuyuki Inagaki, Nobuyuki Takemura, Shinichi Matsumoto, Tsuyoshi Tajima, Norio Ohmagari, Kumiko Ajima, Tadashi Takaki, Yzumi Yamashita, Koya Shinohara, Hiroshi Kajio, Takuya Awata, Masayuki Shimoda","doi":"10.1111/jdi.13996","DOIUrl":"https://doi.org/10.1111/jdi.13996","url":null,"abstract":"<p>Pancreatic islet transplantation is a β-cell replacement therapy for people with insulin-deficient diabetes who have difficulty in glycemic control and suffer from frequent severe hypoglycemia. However, the number of islet transplantations carried out is still limited in Asia. We report a case of allogeneic islet transplantation in a 45-year-old Japanese man with type 1 diabetes. Although the islet transplantation was successfully carried out, graft loss was observed on the 18th day. Immunosuppressants were used in accordance with the protocol, and donor-specific anti-human leukocyte antigen antibodies were not detected. Autoimmunity relapse was also not observed. However, the patient had a high titer of anti-glutamic acid decarboxylase antibody from before the islet transplantation, and autoimmunity might thus have affected the β-cells in the transplanted islet. The evidence is still scarce to reach conclusions, and further data accumulation is required to enable proper patient selection before islet transplantation.</p>","PeriodicalId":190,"journal":{"name":"Journal of Diabetes Investigation","volume":"14 5","pages":"725-729"},"PeriodicalIF":3.2,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.13996","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6027201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}