For any type 1 diabetics out there, or anyone interested in some really neat information! I came across this very interesting study that is sure prompting me to have second thoughts! It addresses the question of whether or not beta cells can regenerate after neonatal time of life… I have only read through this once, but there seems to be some clues that will help put pieces together… Going to go ahead and share this now since it was quite exciting to see that YES the cells CAN regenerate! Will share more once I dig deeper, in the meantime hope this is helpful 🙂
Susan Bonner-Weir, Wan-Chun Li, Limor Ouziel-Yahalom, Lili Guo, Gordon C. Weir, Arun Sharma
Diabetes Oct 2010, 59 (10) 2340-2348; DOI: 10.2337/db10-0084
One point which is very interesting… is the following comment regarding those with gastric bypass surgery… sure makes one consider the role our gut plays in health… And in this particular situation how bypassing impacts blood sugar regulation… What are your thoughts?
“Still more evidence suggesting neogenesis in humans comes from a small group patients who develop hypoglycemia after gastric bypass surgery (79). They have been found to have increased β-cell mass and impressive numbers of islet cells within the ducts (Fig. 2A), accompanied by high circulating levels GLP-1, which has been shown to stimulate neogenesis in rodents (8). From these accumulating circumstantial data, one can be more confident that neogenesis is an important process in humans”.
Are you thinking what I am thinking? There must be something in the area which was by-passed that is having an adverse effect on insulin production and the islet cells…. So what roadblock did that bypass remove???? Hmmm… is this another connection to my post “Microbiome“?
|Neonates||Islet mass growth from cytokeratin+ cells at periphery of islets; β-cell mass determinants measured, and mathematical modeling||Bouwens et al. (21); Wang et al. (89); Finegood et al. (5); Scaglia et al. (6); Bonner-Weir et al. (22)|
|Neonatal STZ||Appearance of small islet clusters associated with ducts||Portha and colleagues (90)|
|Duct ligation||Appearance of small islet clusters associated with ducts||Edstrom (50)|
|Wang et al. (32)|
|Duct ligation + gastrin||Appearance of small islet clusters associated with ducts||Rooman et al. (52)|
|Pancreatectomy (90%)||New lobe formation with new islets, enhanced replication too||Bonner-Weir and colleagues (31, 38)|
|Zucker fatty and Zucker fatty diabetic||Increased small islet clusters associated with ducts||Pick et al. (91)|
|Zucker fatty rats||Increased small islets associated with ducts, increased number islets||Jetton et al. (44)|
|20% glucose infusion (48 h)||Increased small islet clusters associated with ducts||Jetton et al. (92)|
|Exendin 4||Increased hormone+ cells in ducts||Xu et al. (8)|
|Soybean trypsin inhibitor||Increased volume of insulin+ cells in ducts||Weaver et al. (33)|
|Early postnatal||Increased number of islets from 1 week to 2 months; lineage tracing of duct-specific promoter birth to 4 weeks||Inada et al. (20); Peng et al. (26)|
|Ductal ligation||Ngn3+ cells in and adjacent to ducts||Xu et al. (19)|
|CAIICreERT lineage tracing||Inada et al. (20)|
|Alloxan perfusion to part of pancreas||Replication in nonperfused part and neogenesis in perfused||Waguri et al. (34)|
|Alloxan + betacellulin||Increased ICC/mm2 pancreas||Yamamoto et al. (93)|
|Alloxan + adv-betacellulin||Significantly increased insulin+ duct cells||Tokui et al. (94)|
|Alloxan + EGF and gastrin||Significantly increased insulin+ duct cells||Rooman and Bouwens (95)|
|Pancreatectomy (60%)||Increased small clusters before β-cell proliferation; FOXM1 necessary for proliferation but for not neogenesis||Peshavaria et al. (46); Ackermann Misfeldt et al. (47)|
|Retroductal adv-GFP (neonatal)||GFP in islets over first 2 weeks||Peng et al. (26)|
|Metallothionen:TGF-α × Ins:gastrin||Insulin+ cells in metaplastic ducts, increased islets||Wang et al. (37)|
|RIP:interferon-ψ||Increased insulin+ clusters in ducts||Gu and Sarvetnick (36)|
|NeuroD-null mice||10% duct in null mice had “budding” insulin+ cells||Huang et al. (96)|
|Glucagon:Pax4||Reprogramming of α- to β-cells and replenishment of α from ducts||Collombat et al. (30)|
|Obese minipig, after 1 of year age||Increased islet numbers but same mean volume of islets||Larsen et al. (14)|
|Autopsied pancreas, birth to age 20 years||After 12 years, most 0.5–1.2% insulin+ duct cells, some none||Meier et al. (62)|
|Donor pancreas, aged 7–70 years||Unchanged low level of neogenesis from 7 to 70 years||Reers et al. (65)|
|Autopsied, control subjects||Obese 1.2% insulin+ duct cells but lean 0.6 ± 0.2% insulin+ duct cells||Meier and colleagues (66, 74)|
|Autopsied, chronic pancreatitis||Significantly increased glucagon+ or insulin+ duct cells||Phillips et al. (76)|
|Biopsied failed pancreatic transplant||Increased insulin+ ducts in transplants with recurrent autoimmunity||Martin-Pagola et al. (78)|
|Pregnancy||Increased β-cells with no change in replication, cell size, or apoptosis frequency; increased insulin+ duct cells and very small islets||Butler et al. (15)|
Chart is from the above study and can be found at this link.
Would love to hear your thoughts!