Sugar for the type 1 diabetic

[zeropercent21]

When Ray Peat says sugar is good for a diabetic person, is he referring to both type 1 and type 2 diabetic people, or just type 2? I just got into an argument with a friend who's a dietician, and she says that if you give a banana to a type 1 diabetic person he would go into coma and die.

How exactly is sugar good for the diabetic? I know the basics of it, but I just want to be better prepared in case I debate her again.

 

[j.]

Sugar issues

Glucose and sucrose for diabetes

 

[RRT]

An unripened banana is mostly starch and wouldn't be a good choice for a diabetic or non diabetic. Bananas can also be high in serotonin and possibly allergenic.

Clin Exp Allergy. 1999 May;29(5):673-80.
Isolation and characterization of major banana allergens: identification as fruit class I chitinases.
Sanchez-Monge R, Blanco C, Díaz-Perales A, Collada C, Carrillo T, Aragoncillo C, Salcedo G.

Sugar lowers free fatty acids, allowing for the conversion (or "streaming") of alpha cells into insulin-producing beta cells. Free "essential" fatty acids destroy beta cells.

Stem Cells. 2010 Sep;28(9):1630-8.
Pancreatic β-cell neogenesis by direct conversion from mature α-cells.
Chung CH, Hao E, Piran R, Keinan E, Levine F.
Because type 1 and type 2 diabetes are characterized by loss of β-cells, β-cell regeneration has garnered great interest as an approach to diabetes therapy. Here, we developed a new model of β-cell regeneration, combining pancreatic duct ligation (PDL) with elimination of pre-existing β-cells with alloxan. In this model, in which virtually all β-cells observed are neogenic, large numbers of β-cells were generated within 2 weeks. Strikingly, the neogenic β-cells arose primarily from α-cells. α-cell proliferation was prominent following PDL plus alloxan, providing a large pool of precursors, but we found that β-cells could form from α-cells by direct conversion with or without intervening cell division. Thus, classical asymmetric division was not a required feature of the process of α- to β-cell conversion. Intermediate cells coexpressing α-cell- and β-cell-specific markers appeared within the first week following PDL plus alloxan, declining gradually in number by 2 weeks as β-cells with a mature phenotype, as defined by lack of glucagon and expression of MafA, became predominant. In summary, these data revealed a novel function of α-cells as β-cell progenitors. The high efficiency and rapidity of this process make it attractive for performing the studies required to gain the mechanistic understanding of the process of α- to β-cell conversion that will be required for eventual clinical translation as a therapy for diabetes.

Trends Endocrinol Metab. 2011 Jan;22(1):34-43. Epub 2010 Nov 8.
β-cell regeneration: the pancreatic intrinsic faculty.
Desgraz R, Bonal C, Herrera PL.
Type I diabetes (T1D) patients rely on cumbersome chronic injections of insulin, making the development of alternate durable treatments a priority. The ability of the pancreas to generate new β-cells has been described in experimental diabetes models and, importantly, in infants with T1D. Here we discuss recent advances in identifying the origin of new β-cells after pancreatic injury, with and without inflammation, revealing a surprising degree of cell plasticity in the mature pancreas. In particular, the inducible selective near-total destruction of β-cells in healthy adult mice uncovers the intrinsic capacity of differentiated pancreatic cells to spontaneously reprogram to produce insulin. This opens new therapeutic possibilities because it implies that β-cells can differentiate endogenously, in depleted adults, from heterologous origins.

Bioessays. 2010 Oct;32(10):881-4. doi: 10.1002/bies.201000074. Epub 2010 Aug 27.
A new paradigm in cell therapy for diabetes: turning pancreatic α-cells into β-cells.
Sangan CB, Tosh D.
Cell therapy means treating diseases with the body’s own cells. One of the cell types most in demand for therapeutic purposes is the pancreatic β-cell. This is because diabetes is one of the major healthcare problems in the world. Diabetes can be treated by islet transplantation but the major limitation is the shortage of organ donors. To overcome the shortfall in donors, alternative sources of pancreatic β-cells must be found. Potential sources include embryonic or adult stem cells or, from existing β-cells. There is now a startling new addition to this list of therapies: the pancreatic α-cell. Thorel and colleagues recently showed that under circumstances of extreme pancreatic β-cell loss, α-cells may serve to replenish the insulin-producing compartment. This conversion of α-cells to β-cells represents an example of transdifferentiation. Understanding the molecular basis for transdifferentiation may help to enhance the generation of β-cells for the treatment of diabetes.

Diabetes. 2012 Mar;61(3):632-41. Epub 2012 Feb 14.
Free fatty acids block glucose-induced β-cell proliferation in mice by inducing cell cycle inhibitors p16 and p18.
Pascoe J, Hollern D, Stamateris R, Abbasi M, Romano LC, Zou B, O’Donnell CP, Garcia-Ocana A, Alonso LC.
Pancreatic β-cell proliferation is infrequent in adult humans and is not increased in type 2 diabetes despite obesity and insulin resistance, suggesting the existence of inhibitory factors. Free fatty acids (FFAs) may influence proliferation. In order to test whether FFAs restrict β-cell proliferation in vivo, mice were intravenously infused with saline, Liposyn II, glucose, or both, continuously for 4 days. Lipid infusion did not alter basal β-cell proliferation, but blocked glucose-stimulated proliferation, without inducing excess β-cell death. In vitro exposure to FFAs inhibited proliferation in both primary mouse β-cells and in rat insulinoma (INS-1) cells, indicating a direct effect on β-cells. Two of the fatty acids present in Liposyn II, linoleic acid and palmitic acid, both reduced proliferation. FFAs did not interfere with cyclin D2 induction or nuclear localization by glucose, but increased expression of inhibitor of cyclin dependent kinase 4 (INK4) family cell cycle inhibitors p16 and p18. Knockdown of either p16 or p18 rescued the antiproliferative effect of FFAs. These data provide evidence for a novel antiproliferative form of β-cell glucolipotoxicity: FFAs restrain glucose-stimulated β-cell proliferation in vivo and in vitro through cell cycle inhibitors p16 and p18. If FFAs reduce proliferation induced by obesity and insulin resistance, targeting this pathway may lead to new treatment approaches to prevent diabetes.

Endocrine. 2011 Apr;39(2):128-38. Epub 2010 Dec 15.
Long-term exposure of INS-1 rat insulinoma cells to linoleic acid and glucose in vitro affects cell viability and function through mitochondrial-mediated pathways.
Tuo Y, Wang D, Li S, Chen C.
Obesity with excessive levels of circulating free fatty acids (FFAs) is tightly linked to the incidence of type 2 diabetes. Insulin resistance of peripheral tissues and pancreatic β-cell dysfunction are two major pathological changes in diabetes and both are facilitated by excessive levels of FFAs and/or glucose. To gain insight into the mitochondrial-mediated mechanisms by which long-term exposure of INS-1 cells to excess FFAs causes β-cell dysfunction, the effects of the unsaturated FFA linoleic acid (C 18:2, n-6) on rat insulinoma INS-1 β cells was investigated. INS-1 cells were incubated with 0, 50, 250 or 500 μM linoleic acid/0.5% (w/v) BSA for 48 h under culture conditions of normal (11.1 mM) or high (25 mM) glucose in serum-free RPMI-1640 medium. Cell viability, apoptosis, glucose-stimulated insulin secretion, Bcl-2, and Bax gene expression levels, mitochondrial membrane potential and cytochrome c release were examined. Linoleic acid 500 μM significantly suppressed cell viability and induced apoptosis when administered in 11.1 and 25 mM glucose culture medium. Compared with control, linoleic acid 500 μM significantly increased Bax expression in 25 mM glucose culture medium but not in 11.1 mM glucose culture medium. Linoleic acid also dose-dependently reduced mitochondrial membrane potential (ΔΨm) and significantly promoted cytochrome c release from mitochondria in both 11.1 mM glucose and 25 mM glucose culture medium, further reducing glucose-stimulated insulin secretion, which is dependent on normal mitochondrial function. With the increase in glucose levels in culture medium, INS-1 β-cell insulin secretion function was deteriorated further. The results of this study indicate that chronic exposure to linoleic acid-induced β-cell dysfunction and apoptosis, which involved a mitochondrial-mediated signal pathway, and increased glucose levels enhanced linoleic acid-induced β-cell dysfunction.