Although I guess in this case I already know?
So it’s poster time. Get to 670 in the Islet area and come have a chat. Here’s my abstract if you’ve not check it out.
Recent studies have shown that increased inflammation plays a role in the pathogenesis of Type 2 Diabetes (T2D). Circulating levels of pro-inflammatory cytokines are increased in patients suffering from T2D, and metabolic tissues including skeletal muscle and adipose tissue display increased infiltration by inflammatory cells. T2D is characterised by insulin resistance, coupled with decreased insulin secretion, and inflammation is thought to play a role in regulating both. We set out to investigate the effects of inflammation on the possible role of factors secreted from skeletal muscle (myokines) on influencing pancreatic cell function. Skeletal muscle biopsies were taken from T2D and non-diabetic (ND) patients, satellite cells were isolated, propagated, and differentiated into myotubes (SMCs). After differentiation, conditioned media (CM) was collected. The rodent pancreatic β cell line, INS-1 was exposed to this media (25% (v/v); 2x concentrated) for 24 hours prior to determination of cell viability, insulin content and glucose-stimulated insulin secretion (GSIS). GSIS was similarly unaffected by CM from ND and T2D SMCs; treatment with 16.5mM glucose consistently increased insulin secretion by 130-150% over 2.5mM glucose treatment. Seeing that inflammation is increased in T2D, we attempted to create the same state in SMCs using lipopolysacharide (LPS), a bacterial endotoxin capable of inducing pro-inflammatory pathways. SMCs were also treated with a combination of insulin, palmitate and glucose at levels observed in the circulation of T2D subjects, to mimic the “metaflammation” seen in T2D. We have previously shown that infectious (LPS) and metaflammation result in different profiles of myokine secretion. After LPS treatment (1 mg/mL, 24 hr), the secretion of multiple pro-inflammatory myokines (including IL-6, IL-8, TNFα, GRO) were increased from both T2D and ND SMCs. Surprisingly, treatment of INS-1 cells with CM from LPS-exposed SMCs had no effect on GSIS. However, while CM collected from ND SMCs after metaflammation also had no effect on GSIS, INS-1 cells treated with CM from T2D SMCs undergoing metaflammation displayed severely impaired GSIS (65.59 ± 5.6% of control; p<0.001) suggesting that T2D muscle plays a role in impairing β cell function. INS-1 cell viability, total insulin levels and IBMX-stimulated insulin secretion were all unaffected by treatment with ND or T2D CM. The identity of specific factor(s) unique to T2D SMCs capable of causing the decrease in GSIS seen here has yet to be determined, while potential roles for several factors often linked to pancreatic dysfunction (e.g. TNFα and IL-1β) have been ruled out. In conclusion, our results suggest a specific dysfunction in the pathway to GSIS that was induced by the myokine response of T2D muscle cells to a metabolic environment characteristic of T2D.
I have a bunch of graphs and things that explain it all a bit better. They’re even in colour, and as a Englishman you cannot imagine how it was for me to jazz up my poster. Normally my posters and presentations are just white and black (or purple as that was Mancheter’s colours) but this one is full of stuff. We’ve got red and blue, yellow and green, and even some orange.
And yeah it probably clashes.
Today’s quote is from Their/They’re/There (probably Evan Weiss).