Black People May Have Different Mechanism Behind Type 2 Diabetes Compared With White People

Becky McCall

June 28, 2019

Type 2 diabetes in black people appears to be driven by a different mechanism to the conventional concept of visceral fat deposition generating insulin resistance, as largely determined by a research history in the white European population. This conclusion from a new study has potentially widescale implications for disease management.

The results suggest that an independent relationship between glucose and lipid metabolism may exist within the development of type 2 diabetes in this ethnic group.

Lead researcher, Louise Goff, PhD, from King's College London, explained the finding. "We actually found that there is no difference in insulin sensitivity [or conversely resistance] between white and black people with early type 2 diabetes," she said. However, she added that they did see clear differences in relation to fat storage and insulin resistance.

"The visceral fat is much lower in the black group than in the white one. Despite having equal insulin resistance to white men, they don't seem to get this through visceral fat and for some reason they seem to be protected from storing internal fat, which is fascinating. This is a paradox – loads of type 2 diabetes in this population but limited internal fat," she remarked. "The conventional viewpoint of visceral fat as the driving mechanism does not apply to black African men."

Dr Goff emphasised that the finding implied that people of black African origin might be getting poorer care because understanding of type 2 diabetes physiology has been drawn from white populations and applied to everyone. "Many approaches to treating or preventing type 2 diabetes focus on tackling insulin resistance, but if this isn't a driving factor for black African people, then targeting this isn't going to be as effective."

Insulin Resistance Drives High Insulin Levels or Vice Versa? 

For many decades, research in the white population showed that the primary defect in type 2 diabetes was insulin resistance in the muscle and liver cells. The pancreas counteracts this resistance by increasing insulin secretion but over time the beta cells cannot maintain this level of insulin production, and hyperglycaemia results.

More recently, research suggests that the primary defect is earlier than this and lies in the visceral fat tissue, explained Dr Goff. With high calorie intake, subcutaneous adipose tissue can no longer process and store fat, leading to a deposition of fat in and around the organs, for example the liver, pancreas, and muscles. Again, research in the white population, shows how this leads to insulin resistance and failure of the beta cells, so typical of type 2 diabetes.

Reviewing this previous research, Dr Goff found very little consistency in study methods. She noted large cohort studies reporting people with type 2 diabetes to be highly insulin resistant, while other smaller studies reported high insulin exposure. "Taken together, people with type 2 diabetes seem to be more insulin resistant and in response, the pancreas produces more insulin. But the problem with interpreting these data is that measures of insulin resistance were very indirect, leading to a misplaced generalisation of type 2 diabetes mechanisms."

Black African people are up to three times more likely to develop type 2 diabetes than white European people. In the study led by Dr Goff, insulin resistance was measured in men with type 2 diabetes, 18 of whom were black African and 15 white European. Dr Goff hypothesised that, in those with early type 2 diabetes, black African men would have greater hepatic and adipose tissue insulin sensitivity, compared with white European men, because of their reduced visceral fat.

Comprehensive Study

"We believe this is the most comprehensive study to date where we use gold standard measures of insulin resistance across the body but also [in] the organs – liver, muscle and adipose tissue," reported Dr Goff in an interview with Medscape News UK.

All the men received fixed doses of glucose over a 4 hour period and then the researchers looked at how much insulin they produced in response. The groups were matched for age and body mass index (BMI), as well as duration of diabetes and HbA1c.

Gold standard measures of insulin secretion by the pancreas were also used.  Magnetic resonance imaging (MRI) provided a measure of visceral fat storage in and around the liver, skeletal muscles, and pancreas. "This is the first study to put all these measures together in one population, and in this respect our study was unique [in] providing robust data," Dr Goff said.

No ethnic differences were seen in whole body, skeletal muscle, liver or adipose tissue insulin sensitivity between black men and white men. This finding occurred in the presence of lower visceral fat in the black men (3.72 vs 5.68 kg [mean difference −1.96, 95% CI −3.30, 0.62]; p = 0.01). An association between skeletal muscle and adipose tissue insulin sensitivity was seen in white men but not in black men.

Commenting on their results compared with those in the literature, Dr Goff said that previous reports of high insulin resistance in black African people were most likely due to indirect methods of measuring resistance, and partly due to diverse study populations relating to obesity levels and/or age. "When we controlled for these features we found black men were no more insulin resistant than white [men]."

The implication of this finding is that current management of type 2 diabetes, which involves medications that encourage the pancreas to produce more insulin, might not provide optimal management in black people, Dr Goff pointed out. "We need to understand the principal mechanism in the black population to then know what the best disease management options are and whether there are new drug targets."

Dr Goff and her team are repeating the same protocol in healthy men, and in men with pre-diabetes to try and understand how this develops and to understand defects early on.

Dr Elizabeth Robertson, director of research at Diabetes UK, which funded the study, commented on the work. "There is still more to be done in terms of understanding how and why type 2 diabetes develops differently in black African people, and why this puts them at increased risk. But this research helps us to build on our current knowledge, so we can improve care even further and move towards more personalised type 2 diabetes treatment and prevention strategies for people of BAME [black, Asian and minority ethnic] backgrounds in the future."

COI: Dr Goff has no relevant disclosures.

Published in this week's edition of Diabetologia. The study was sponsored by Diabetes UK.

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