Del Prato S, Riva F, Devidé A, Nosadini R, Fedele D, Tiengo A
Acta Diabetol Lat. 1980 Apr-Jun;17(2):111-8. doi: 10.1007/BF02580992.
In three groups of patients with insulin-dependent diabetes following total (n = 5) or partial (n = 5) pancreatectomy or chronic pancreatitis (n = 7) and in a group of idiopathic diabetics, ketogenic capacity following insulin withdrawal and during a 24-h fast was studied. Basal glucagon values were significantly increased in all diabetic groups with no significant intergroup differences. Basal ketone body values and their increase during starvation and insulin withdrawal were high and not different in totally pancreatectomized and primary diabetics, both showing unmeasurable C-peptide levels. On the contrary, ketogenesis was reduced in partially pancreatectomized and in pancreatitis diabetics with persistent levels of C-peptide. Our data confirmed the persistence of immunoreactive glucagon after pancreatectomy and demonstrated that ketogenesis is not suppressed in pancreatectomized diabetics and depends above all on residual B-cell function. A possible ketogenic effect of extra-pancreatic glucagon-like substances cannot be excluded.
对三组胰岛素依赖型糖尿病患者进行了研究，这三组患者分别为全胰腺切除术后（n = 5）、部分胰腺切除术后（n = 5）或患有慢性胰腺炎（n = 7），还有一组特发性糖尿病患者，研究了胰岛素停用后以及24小时禁食期间的生酮能力。所有糖尿病组的基础胰高血糖素值均显著升高，组间无显著差异。基础酮体值及其在饥饿和胰岛素停用期间的增加在全胰腺切除患者和原发性糖尿病患者中较高且无差异，二者的C肽水平均无法测量。相反，部分胰腺切除患者和患有胰腺炎的糖尿病患者的酮生成减少，其C肽水平持续存在。我们的数据证实了胰腺切除术后免疫反应性胰高血糖素的持续存在，并表明胰腺切除术后糖尿病患者的酮生成并未受到抑制，且主要取决于残余B细胞功能。不能排除胰腺外胰高血糖素样物质可能的生酮作用。
